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Volume IV: 

Cardiovascular 

and 

Cerebrovascular 

Disease 

Part 2 




Report of the 
Secretary's Task 
Force on 



Black & 

Minority 

Health 



U.S. Department of Health and 
Human Services 



muujrric^Y 



Volume IV: 

Cardiovascular 

and 

Cerebrovascular 

Disease 

Part 2 



Report of the 
Secretary's Task 
Force on 



Black & 

Minority 

Health 



U.S. Department of Health and 
Human Services 

January 1986 



SUBCOMMITTEE ON CARDIOVASCULAR AND CEREBROVASCULAR DISEASES 

TABLE OF CONTENTS 
PART 2 
Supporting Papers 

1. Shiriki K. Kumanyika, Daniel D. Savage: Ischemic Heart 

Disease Risk Factors in Black Americans 229 

2. Lucile L. Adams, Laurence 0. Watkins , Lewis H. Kuller, 
Daniel D. Savage, Richard Donahue, Ronald E. T;aPorte: 
Relationship of Social Class to Coronary Disease Risk 
Factors in Blacks: Implications of Social Mobility for 

Risk Factor Change 285 

3. Hector F. Myers: Coronary Heart Disease in Black Populations: 

Current Research, Treatment, and Prevention Needs 303 

4. Melford J. Henderson, Daniel D. Savage: Prevalence and 
Incidence of Ischemic Heart Disease in United States' 

Black and White Populations 347 

5. Helen P. Hazuda: Differences in Socioeconomic Status 
and Acculturation among Mexican Americans and Risk of 
Cardiovascular Disease 367 

6. Shiriki K. Kumanyika, Daniel D. Savage: Ischemic Heart 

Disease Risk Factors in Hispanic Americans ........ 393 

7. Shiriki K. Kumanyika, Daniel D. Savage: Ischemic Heart ; 

Disease Risk Factors in Asian/Pacific Islander Americans .... 415 

8. Shiriki K. Kumanyika, Daniel D. Savage: Ischemic Heart 
Disease Risk Factors "In American Indians and Alaska 

Natives 445 

9. Lewis H. Kuller: Stroke Report 477 



Ischemic Heart Disease 
Risk Factors in Black 
Americans 




mi:,v.-HiL-y»-ii,!>if:aMJa^^^^.rj>f-jTOEas 




Shiriki K. Kumanyika, Ph.D., M.P.H. 

Assistant Professor 

Department of Epidemiology 

Johns Hopkins School of Hygiene and Public Health 

Baltimore, Maryland 

Daniel D. Savage, M.D., Ph.D. 

Medical Advisor 

National Center for Health Statistics 

Hyattsville, Maryland 



TABLE OF CONTENTS 

1.0 CIGARETTE SMOKING 232 

1.1 Prevalence 232 

1.1.1 Data Sources 

1.1.2 Black/white differences in prevalence of current and 

heavy smoking: 1965-1982 

1.1.2.1 Current Smoking: Men 

1.1.2.2 Heavy Smoking: Men 

1.1.2.3 Current Smoking: Women 

1.1.2.4 Heavy Smoking : Women 

1.2 Impact 239 

1.2.1 Data Sources 

1.2.2 Findings 

1.3 Implications 244 

1.4 Recommendations 245 

1.5 References 246 

2.0 CHOLESTEROL 248 

2 . 1 Data Sources 248 

2.2 Findings 250 

2.2.1 Total and lipoprotein cholesterol comparisons among 

black and white men 

2.2.1.1 Total cholesterol: men 

2.2.1.2 Lipoprotein cholesterol: men 

2.2.2 Total and lipoprotein cholesterol comparisons among 

black and white women 

2.2.2.1 Total cholesterol: women 

2.2.2.2 Lipoprotein cholesterol: women 

2.2.3 Basis of lipoprotein cholesterol differences in blacks 

and whites 

2.2.4 Impact of cholesterol-associated risk on CHD 

disparities between blacks and whites 

2.2.5 Intervention studies 



229 



2.3 Recommendation 262 

2.4 References 263 

3.0 ELEVATED BLOOD PRESSURE AND HYPERTENSION 267 

3.1 Prevalence 267 

3.1.1 Data Sources 

3.1.2 Findings 

3.1.2.1 Elevated Blood Pressure and Hypertension in Black and 

White Men, 1960-1980 

3.1.2.2 Demographic Patterns : Men 

3.1.2.3 Prevalence of Elevated Blood Pressure and Hypertension 

in Black and White Women, 1960-1980. 

3.1.2.4 Demographic Patterns : Women 

3.2 Left Ventricular Hypertrophy 275 

3.3 References 279 

4.0 CONCLUSION 282 



230 



INTRODUCTION 

The Task Force on Black and Minority Health Subcommittee on 
Cardiovascular and Cerebrovascular Diseases is attempting to understand and 
document the extent and determinants of racial disparities in 
cardiovascular and cerebrovascular diseases. This paper focuses on black 
Americans and on the ischemic heart disease (IHD) component of 
cardiovascular morbidity and mortality. IHD prevalence and incidence are 
addressed in a separate paper (Henderson and Savage) . Data and issues 
relating to standard and other IHD risk factors are considered here. The 
specific objectives of this paper are to summarize and evaluate the 
available information on IHD risk factors in black men and women and to 
discuss implications of the data for the DHHS Task Force on Black and 
Minority Health. 

The scope of this paper is broad due to the need to cover several 
different risk factors in both black men and women and the need to scan a 
large literature on cardiovascular disease in whites for the relatively 
limited information on minority populations. For practical purposes 
related to the division of responsibilities among consultants to the Task 
Force, subjects which would be coherently considered together have been 
separated. Thus, IHD outcomes are discussed in relative isolation from 
cerebrovascular disease and diabetes. Also, an attempt is made to examine 
separately risk factors which occur in clusters and which interact. Some 
important factors such as obesity have already been incorportated into the 
subcommittee report by Dr. Watkins and, to avoid duplication of effort, 
have not been discussed here at length. The assumption is that a complete 
multivariate picture will emerge from a synthesis of several papers, by the 
Subcommittee and Task Force members . 

Based on the impression of Henderson and Savage from their review of 
prevalence and incidence of IHD in black Americans, the context for 
consideration of IHD risk among blacks has been as follows: 

" In black men, up to between ages 55 and 65, the prevalence- 
incidence of IHD appears to be similar to that in white men. 

" After about age 60-65 (the range of the average life span of 
black men), black men have a substantially lower prevalence/ 
incidence of IHD than white men (average life span 65 to 71 
years) . 

" IHD prevalence/incidence in black women is similar to or 
greater than that of white women, with no crossover. 



Cigarette smoking, cholesterol, hypertension, and diabetes are the 
standard risk factors for IHD. References describing prevalence, impact, 
and intervention aspects of three of these determinants have been selected 
and evaluated for implications related to the Task Force Mission. 
Diabetes' risks have been addressed by the Diabetes Subcommittee of the 



231 



Task Force. Left ventricular hypertrophy (LVH) (which is highly prevalent 
in blacks relative to whites) is discussed as a putative independent IHD 
risk factor. Emphasis has been given to recent references (1980 to 
present), with attention to time trends, in order to make the scope 
manageable and also to provide sufficiently timely perspectives for action. 

1.0 CIGARETTE SMOKING AMONG BLACK AMERICANS 

1.1 PREVALENCE 

1.1.1 Data Sources 

National probability estimates of the prevalence of cigarette smoking 
among black adult men and women during and between 1965-1983 are available 
from the National Health Interview Survey (NHIS), the National Health 
Examination Surveys (NHANES), and the Centers for Disease Control 
Behavioral Risk Factor Survey (CDC-BRFS) (1-9) . NHIS and NHANES data are 
from in-person interviews. CDC data are from a telephone survey. All of 
these sources provide estimates of rates of current smoking for the years 
covered. In addition, NHIS sources provide data on number of cigarettes 
smoked per day for current smokers (mean or categorical distribution) , 
percentages of former smokers, smokers who have attempted to stop smoking, 
length of time since stopping, and tar and nicotine levels. NHANES 
provides percentages of heavy smokers, defined as 25 cigarettes or more per 
day. All sources provide comparison data for whites. However, NHIS and 
NHANES include Mexican-Americans in the white category. 

The treatment of age in published tables varies. NHIS reports use 
20-24, 25-34, and 35-44 years, with 45-54 and 55-64 years either separate 
or combined as 45-64. NHANES data are reported for decades between 25 and 
74 years. Only age-adjusted data were available for some black-white 
comparisons in both NHIS and NHANES. CDC data are reported for the 
categories 25-44, 45-64 and 65+ years. Time trends can be examined within 
NHIS and NHANES data, but only on a cross-sectional basis. No direct 
comparisons across data bases are appropriate due to the different sampling 
and data collection protocols. All smoking data in these surveys are 
self-reported (i.e., they have not been validated by biochemical tests). 

In addition, estimates of smoking status of black and white men and 
women in several large, widely-based samples were identified: 

" American Cancer Society data on smoking status of 1 million men and 
women (black n=25,000) over age 40, screened in 25 states in 1959 for 
prospective follow-up (10) . 

" American Health Foundation data on smoking status by education and 
black or white race among 23,953 (black n=3628) men and women in nine U.S. 
cities (major east, west, north, south population centers), 1970-75 and 
1976-80 (cross-sectional). Seventy percent or more of this population was 
over 45 years of age (range 20-80). The population consisted of 
hospitalized men and women diagnosed with nontobacco-related conditions 
and selected to be age-matched controls of adult cancer cases. Data for 



232 



the four race-sex groups are presented for each of the two time 

periods within two educational categories (high school or less and college 

or more) (11) . 

" Multiple Risk Factor Intervention Trial (MRFIT) data on smoking status 
of 348,874 (black n=23,490) men ages 35-57 screened at 22 clinical centers 
in 18 U.S. cities during 1973-75 (12). 

" MRFIT data on smoking status of 12,866 (black n=931) men ages 35-57 
with risk scores in the upper 10-15% of the Framingham distribution who 
were screened during 1973-75 and randomized to a specialized intervention 
or to control. Smoking status at screening and after intervention 
(thiocyanate adjusted) are presented (13). 

" Hypertension Detection and Follow-Up Program (HDFP) data on smoking 
status by systolic and diastolic blood pressure levels for 59,610 (black 
n=18,127) men and women ages 30-69 years screened during 1973-74 in 14 U.S. 
communities. Data for each sex-race group are presented for several blood 
pressure categories and by medication use with four age categories and 
age-adjustment (14). 



1.1.2 Black/White Differences in Prevalence of Current and Heavy 
Smoking: 1965 - 1982 

1.1.2.1 Current Smoking: Men 

Age-adjusted national estimates of prevalence of current smokers 
indicated an 8-9% higher prevalence of smoking in black compared to white 
men (age >=20 years) in 1965, 1976, and 1980--although rates for both black 
and white men had declined by approximately 14% (4) . The direction of the 
difference in smoking rates between black and white men was the same in all 
data sources reviewed, i.e., rates for black men were higher than those for 
white men. However, the size of the difference varied from 2% in the 
American Cancer Society study (10) to 17-18% in college-educated 
hospitalized cancer controls (11) and in the HDFP screenees (14). 

In the NHIS and NHANES reports (6,7), the size of the black-white 
differential in male smoking rates remained relatively constant between 
1970 and 1980 (less than 1% change in the difference between the two rates) 
(Table S-1). In the hospitalized cancer control population (11) with a 
high school education or less, the difference in black and white male 
smoking rates increased by 5% (black rates dropped less than white rates). 
In contrast, smoking rates in college educated men in this population 
showed a 6.5% narrowing of the black/white difference: rates among 
college-educated black men dropped more than those of the white men. 
Longitudinal data on the MRFIT Usual Care group showed a slight increase in 
the black/white difference (from 5.7% to 7.4%) between the time of 
screening 1973-75 and follow-up six years later. 



233 



Table S-1. Selected comparisons of self -reported smoking rates 
for black and white men, 1965-1980 (% current smokers in 
population subgroup) . 



REF/ AGE 1 
SOURCE RANGE | 


1965 


t 1 

1 


1971-75 1 


1976 1 


1976-80 1 


1980 


1 CHANGE 
1 


(6) >=20 
NHIS years 


BM 
WM 


59. 

51. 


6 
3 




50.1 
41.0 




44. 
37. 


.9 

,1 


-14.7 
-14.2 


(7) 25-74 
NHANES 


BM 
WM 






55.4 
43.6 




50.7 
39.6 






-4.7 
-4.0 


(11) 20-80 
hospitalized 
<=high sch 


BM 
WM 






59.4 
47.5 




55.1 
37.8 






-4.3 
-9.7 


>=college 


BM 
WM 






54.2 
35.5 




36.5 
25.3 






-15.7 
-10.2 


(12) 35-57 
MRFIT 


BM 
WM 






50.0 
35.9 













screenees 



(14) 30-69 


BM 


49.2 


HDFP meds 


WM 


30.6 


no meds 


BM 


57.1 




WM 


39.2 



Age-specific tabulations of national probability estimates of smoking 
rates in men show the lowest rates in men over 65, next lowest among men 
45-65, and higher rates among men 20-44. Rates in 25-34 year-old men tend 
to be the highest. Comparison of black and white rates indicate that the 
higher prevalence of smoking in black vs. white men is seen in every age 
group in data for 1965, 1976, and 1980. A relatively small black/white 
difference for 35-44 year-old men in 1980 (44.2% vs. 42.2%) may indicate a 
changing pattern for this birth cohort (6). 

Age-specific data for blacks but not whites are given in one of the 
available NHANES reports (7). Race-specific data from the CDC-BRFS for the 
25-44, 45-64, and 65+ age-groups are included in Carter Center Report (8) 
as the basis for calculating attributable risks associated with smoking. 
These data (see below) do not fit the overall picture indicated by NHIS and 



234 



NHANES regarding smoking prevalence differences between black and 
white men--in either the size of the black/white difference or the 
prevalence of smoking in black men over 65 (NHIS 27.9% in 1980 (6) and 
NHANES II 26.9 in 1976-80 (7) as compared to 39.2 in the CDC data for 65+ 
black men. 



Table S-2. Percent of current smokers in the NHIS (1980) and 
CDC-BRFS (1982) U.S. population samples, 
black and white men ages 25 years and over 



NHIS 



CDC 



25-34 35-44 45-64 



65+ 



25-44 45-64 



65+ 



BM 


52, 


.0 


44, 


.2 


48, 


,8 


27, 


.9 


39 


.4 


38, 


.3 


39, 


.2 


WM 


42, 


.0 


42, 


.4 


40, 


.6 


16, 


.6 


37 


.8 


36, 


.5 


16, 


.4 



At the present writing, two important aspects of the CDC data are 
unclear: 1) the socioeconomic distribution of the sample (given that all 
respondents were contacted by telephone; and 2) the upper age limit of the 
sample compared to NHIS (actually the upper limit of NHIS is unclear; only 
NHANES data clearly designate the upper age limit). The definition of 
"current smoking" is not likely to differ greatly between surveys. 

If the CDC data are comparable to that from NHANES or NHIS, then the 
CDC prevalence rates can be interpreted as the more current data as 
compared to the pre-1981 estimates from the other two sources. As 
indicated above, with the exception of black males over 65 years, the CDC 
rates are lower than those reported for men of similar ages in 1980. Thus, 
the CDC rates are plausible as evidence of a continued decline in smoking 
rates in both races and a narrowing of the gap between black and white men 
under age 65. The high rate of smoking in black men over age 65 in the CDC 
data is difficult to interpret. The possible limitations of the CDC data 
should be kept in mind when evaluating the attributable risk calculations, 
presented later in this section, which are based on these smoking 
prevalence rates . 



1.1.2.2 Heavy Smoking 



Men 



NHIS age-adjusted estimates of the percent of adult smokers (age >=20 
years) who smoke 25 or more cigarettes per day show an increase between 
1965 and 1980 in both black and white males. The prevalence of heavy 
smoking is substantially higher among white men compared to black men and 
the increase in heavy smoking rates between 1965 and 1980 is steeper for 
white men (Table S-3) . 



235 



Table S-3. Percentages of smokers or population sub-group 

smoking 25 or more cigarettes per day, black and 
white men, 1965-1980. 

REF/ AGE I 1965 | 1971-75 | 1976 | 1976-80 | 1980 | CHANGE 
SOURCE RANGE | | | | | j 



(6) >=20 


BM 


8, 


.6 




10, 


.8 




13, 


.8 


+5.8 


NHIS * 


WM 


26, 


.0 




33, 


.3 




37, 


.3 


+ 11.3 


(7) 25-74 


BM 






7.5 






8.5 






+ 1.0 


NHANES # 


WM 






16.9 






16.6 






-0.3 


(7a) 35-74 


BM 






5.6 






9.6 






+4.0 


NHANES# 


WM 






17.1 






17.5 






+0.4 


(12) 35-57 


BM 






18.5 




- . 


. - - - 


_ _ . 




. - - 


MRFIT 


WM 






26.9 














screenees 























7o of current smokers 



// % of population subgroup 



NHANES estimates of heavy smoking in the 25-74 year-old population 
--expressed per 100 population (% of population subgroup rather than as a 
proportion of smokers only) --indicate no appreciable change in the 
proportion of heavy smokers in the population. Thus, the increase in the 
percent of heavy smoking in men appears to be relative to the overall 
decline in the number of smokers. The decline in smoking among men has 
been among light (<15 cigarettes per day) and moderate (15-24 cigarettes 
per day) smokers. The NHANES estimates of heavy smoking in the 35-74 year 
old segment of the population do suggest an increase in the number of black 
men who are heavy smokers. Smoking rates in this age-group of men declined 
only slightly (48.7% to 46.5% from 1971-75 to 1976-80) (7a). 

Age-specific data indicate that 35-64 year-old smokers are more likely 
to be heavy smokers than the other age-groups among both black and white 
men (6). Among white men, all age-groups of smokers showed a consistent 
increase in the percent of heavy smokers between 1965 and 1980, with the 
steepest rise in the 35-44 year-old age-group. Among black male smokers, 
although no age-groups show a decline in rates, the age-specific picture of 
changes in heavy smoking among black men is much less consistent than for 
whites and is complicated by inadequate cell sizes for stable estimates in 
the 20-24 and 65+ year age-groups in 1965 and 1976. The age-adjusted 



236 



cross -sectional data are probably misleading as to trends in heavy 
smoking for any age-group or birth cohort of black men. In the NHANES data 
which do give estimates for all decades between 25 and 74, 25-34 year-olds 
show a 7% decrease while 35-44 and 55-64 year-olds show 8 and 7% increases. 

1.1.2.3 Current Smoking: Women 

With the exception of MRFIT, all of the data sources described include 
data for women. Smoking patterns for women are very different from those 
of men. Rates are lower, time trends are different, and consistent 
black-white differentials are not observed. 

Data collected before 1970 (6,10) and after 1976 indicate an equivalent 
or slightly lower prevalence of smoking in black vs. white women (6,7,11) 
(Table S-4) . Between 1971 and 1976 the prevalence of smoking in black 
women was higher in all samples examined (6,7,11,14). Smoking rates of 
black women have decreased to a greater extent than those of white women 
since 1976 in the NHIS and NHANES samples and in both the lower and higher 
educated segments of the American Health Foundation population of 
hospitalized cancer controls (11). 



Table S-4. Selected comparisons of self -reported smoking rates 
for black and white women, 1965-1980 (% current 
smokers in population subgroup) . 

REF/ AGE I 1965 | 1971-75 | 1976 | 1976-80 | 1980 | CHANGE 
SOURCE RANGE | | | | | | 



(6) >=20 


BF 


32, 


.7 




34, 


,7 




30, 


.6 


-2.1 


NHIS 


WF 


34. 


,5 




32, 


,4 




30, 


,0 


-4.5 


(7) 25-74 


BF 






46.2 






31.6 






-14.6 


NHANES 


WF 






34.0 






33.0 






- 1.0 


(11) 20-80 






















hospitalized 


BF 






39.3 






25.0 






-14.3 


<=high sch 


WF 






33. L 






28.0 






- 5.1 


>=college 


BF 
WF 






42.3 
34.1 






26.5 
28.9 






-15.8 
- 5.2 


(14) 30-69 
HDFP meds 


BF 
WF 






29.8 
23.8 






























no meds 


BF 
WF 






38.6 
33.8 

































237 



The age-specific data for women indicate substantially lower prevalence 
of smoking in women age 65 years and older compared with younger women (6) . 
The percent of current smokers among white women (but not for black women) 
age 65 years and over increased sharply between 1965 and 1980. NHANES 
data, which separate 45-54 and 55-64 year-old women, show a substantial 
.break towards lower smoking prevalence rates in black women over age 55 
years . 

CDC and NHIS age-specific data on smoking prevalence in women are shown 
in Table S-5. As seen in the data for men, CDC rates are lower and may be 
evidence of a continuing downward trend. No striking black/white 
differences in prevalence are evident in either data set. If the data sets 
are comparable, then smoking trends in black and white women age 65 years 
and over are changing: rates in black women in this age-group may be 
increasing and those in this age-group of whites decreasing. 



Table S-5. Percent of current smokers in the NHIS (1980) and 
CDC-BRFS (1982) national probability samples, 
black and white women ages 25 and over 



NHIS 



CDC 



25-34 35-44 45-64 



65+ 



25-44 45-64 



65+ 



BF 


34. 


.2 


36 


.5 


34. 


.3 


9 


.4 


30, 


,8 


24, 


.4 


13, 


.6 


WF 


31. 


.6 


35 


.6 


30. 


.6 


17 


.4 


33, 


.4 


31, 


,3 


11, 


.2 



1.1.2.4 Heavy Smoking : Women 

Black/white differences in the prevalence of heavy smoking are 
evident among women and are of the same nature as those observed for men. 
Substantially more white than black women smokers report use of 25 or more 
cigarettes per day. The percentage of heavy smokers among white women 
smokers increased to the same extent as for white men in the NHIS data for 
1965-80. A much lesser increase was observed in black women over these 
three surveys. NHANES estimates of the percentage of heavy smokers among 
25-74 year-old women do not show an appreciable change for either black or 
white women (see Table S-6) . 



238 



Table S-6. Percentages of smokers or population sub-group 

smoking 25 or more cigarettes per day, black and 
white women, 1965-1980. 

REF/ AGE I 1965 | 1971-75 | 1976 | 1976-80 | 1980 [CHANGE 
SOURCE RANGE | j j | | | 



(6) >=20 


BF 


4. 


,6 




5, 


.6 




8.6 + 4.0 


NHIS * 


WF 


13. 


.9 




20, 


.9 




25.2 +11.3 


(7) 25-74 


BF 






3.0 






3.9 


+0.9 


NHANES # 


WF 






7.4 






8.6 


+ 1.2 


(7a) 35-74 


BF 






1.1 






3.5 


+2.4 


NHANES# 


WF 






6.0 






8.2 


+2.2 



% of current smokers 



# % of population subgroup 



Age-specific data for heavy smoking among women indicate that women 
smokers age 20 or less or over age 65 are least likely to fall into the 
heavy smoking category (6) . The increase in percent of white women smokers 
who are heavy smokers between 1965 and 1980 is seen consistently in each 
age-group of white women (6) . Trends across surveys cannot be evaluated in 
the NHIS data for black women heavy smokers due to inadequate numbers in 
several categories. NHANES age-group-specific percentages of heavy smokers 
are available for black women ages 25-54 for 1971-75 and ages 25-74 for 
1976-80 (7). Apparent differences in smoking trends of different birth 
cohorts render general statements about time trends in heavy smoking among 
black women misleading--a situation similar to that observed in the heavy 
smoking data for black men. 

1.2 Impact i 

1.2.1 Data Sources 

Four sources for estimates of the impact of smoking on coronary heart 
disease in nationally-based samples were identified: 

" The American Cancer Society prospective study (10) presents CHD 
mortality ratios for black men and women. Mortality ratios for blacks were 
calculated using deaths for whites in the comparable sex-age-group (5 year 
age-group at entry) as the denominator of "expected" deaths and deaths 
observed in blacks as the numerator. Actual death rates are not presented. 
Dose-response effects of smoking were examined by calculating the ratio of 
deaths for each of three smoking categories to deaths among nonsmokers, 
within race. Mortality ratios of black smokers with and without a history 



239 



of disease were also presented, using rates for white nonsmokers 
with no major disease history as the expected rates. The analysis is based 
on 642 and 487 CHD deaths in 22,000 black males and females 40 years and 
older during a 12 year period of follow-up between 1960 and 1972. Smoking 
categories were: never smoked, 1-9, 10-13, and 20+ cigarettes per day. 
CHD was defined by lCD-7 420.0, 420.1 and 420.2. 

" Kleinman, Feldman, and Monk (National Center for Health Statistics) 
estimated the extent to which the 20% decline in smoking between 1965 and 
1976 could account for the decrease in CHD mortality for men and women 
35-64 years old during the same time period (3) . NHIS population 
percentages in 4 smoking categories were used to estimate expected percent 
change in CHD death rates by each of four dose-response models and for each 
of four risk models. Smoking categories were: 0, <15, 15-24, and >=25 
cigarettes per day- -recognizing that the larger percentage of former 
smokers in the nonsmoking category in 1976 vs. 1965 would lead to some 
degree of overestimation of effects. The dose-response models were: 
constant risk at any dose; logarithmic (risk increases rapidly in the lower 
dose range and then levels off); linear (similar increase in risk with each 
additional cigarette) ; and exponential (higher risk associated with each 
additional cigarette). Risk models were derived from the Veterans', 
American Cancer Society, British Physicians, and Framingham studies. CHD 
was defined by ICD-8 codes 410-413 (1968) extrapolating backwards to cover 
1965, 1966, and 1967. 

" Five year cerebrovascular, CHD, CVD and all-cause mortality (6018 
deaths) among 23,940 black and 325,384 white male MRFIT screenees (12) was 
subjected to logistic regression analyses to determine associations with 
several risk factors, including cigarette smoking. CVD was defined by 
ICD-9 codes 390-459; CHD by codes 410 to 414; cerebrovascular disease by 
codes 430-438. Smoking categories were: nonsmokers, 1-15, 16-25, 26-35 or 
>35 cigarettes per day at the time of screening. 

" The Carter Center Report includes estimates of the CHD deaths, years 
of life lost due to CHD death, and CHD cases attributable to smoking in the 
U.S. population and the proportion of CHD deaths and cases in persons 25 
years or older that could be prevented if cigarette smoking were eliminated 
(8). Cigarette smoking is defined by the CDC 1982 data on percent of 
current smokers, described earlier. Population attributable risk estimates 
were derived from the Risk Factor Update Project logistic regression 
equation (Breslow et al., cited in 8). This equation is similar to the 
Framingham equation but is based on pooled equations for several major CVD 
studies and permits estimates for blacks and whites. CHD death was defined 
by ICDA codes 410-414 using 1980 death rates. 

Each of these analyses carries several assumptions and can only be 
interpreted in light of the risk model, morbidity and mortality data, and 
risk factor patterns which apply. For example, the MRFIT and Carter Center 
analyses of smoking effects hold several competing risk factors, and some 
risk factor interactions constant. The American Cancer Society and NCHS 
analyses do not. The ACS and MRFIT populations are volunteers for health 
risk-related studies and are prospective. Both the NCHS (3) and Carter 



240 



Center (8) reports provide smoking risk estimates for the U.S. 

population but they use smoking prevalence data from two different and not 

necessarily comparable data bases. 

1.2.2 Findings 

The American Cancer Society study (10) demonstrates a significantly 
higher risk of 12-year CHD mortality among black men and women smokers 
under age 65, compared to white men and women nonsmokers in the same age 
range at entry. Higher CHD mortality associated with smoking was seen in 
black men and women both with and without a major disease history. The 
prevalence of smoking was somewhat higher in white men than black men, 
consistent with the higher CHD mortality among the white men (i.e., the 
black-white CHD mortality ratio was less than one for men in all age 
groups). However, certain characteristics of the study sample suggest that 
it was not representative of blacks in the general population. For 
example, the prevalence of smoking was lower among black men compared to 
white men in this sample and the prevalence of major disease was not 
substantially greater in the black men, as might have been expected. The 
sample was geographically broad, but consisted of friends, relatives, and 
neighbors of ACS volunteers. The authors point out that educational levels 
in the sample are higher than those reported in census figures and that 
inner city persons are underrepresented. 

CHD mortality among black women was greater than for white women for 
women ages 40 through 59 at entry. Somewhat more white women than black 
women smoked and were heavy smokers. The prevalence of major disease, as 
defined in this study, was 12% higher among the black women (32% vs. 20%). 
More of the black women were 30% or more overweight (17% vs. 4%). 

The MRFIT screenee population (12) is probably healthier than average 
due both to the use of employment sites for screening and to the fact that 
the highest risk men have been excluded due to enrollment in the randomized 
trial. Individual effects of smoking are considered, i.e., after 
adjustment for other risk categories (age, serum cholesterol concentration, 
diastolic blood pressure level) . Smoking is more prevalent in the black 
men, but they are less heavy smokers. Smoking was associated with a 
significant, similar excess risk of CHD in black and white men in this 
population. This association was not dependent on the presence of heart 
attack or diabetes; removal of such men from the analysis did not alter the 
result. 

Dose response effects of smoking on CHD mortality were positive and 
generally similar in blacks and whites, allowing for some instability of 
cause-specific mortality rates among the relatively small numbers 
contributing to rates for black men in the heavy smoking categories. CHD 
mortality was higher in smokers than nonsmokers among black men with and 
without hypertension and with and without elevated serum cholesterol. 

Kleinman et al. (3) determined the percentage decline in CHD deaths 
for 35-64 year-olds in the U.S. population between 1965 and 1976 which 
could be attributed to a decline in smoking over the same period. 



241 



Estimates are only presented for men, since smoking rates for women did not 
decline significantly in the time period addressed. 

Although four models are used to calculate expected decline in deaths 
associated with changes in smoking patterns, estimates based on the 
"constant risk" model lend themselves to the most straightforward 
interpretation. Estimates with this model are based simply on the 
percentage of current smokers , without regard to average number of 
cigarettes smoked. In black males, changes in smoking prevalence could 
account for 23, 23, and 21 percent of the CHD mortality decline for the 
35-44, 45-54 and 55-64 year-old age-groups, respectively. Comparison 
percentages for white males were 40, 50, and 16%. Thus, changes in smoking 
had less of an impact on the decline in CHD mortality in black as compared 
to white men 35-54 and slightly more of an impact in black men 55-64 years 
old. Results based on the other risk models, which take the number of 
cigarettes smoked into account, show similar results. The factors other 
than smoking which contributed differentially to the decline in CHD 
mortality among black and white men are uncertain. 

The Carter Center Report (8) provides estimates of the number and 
percent of CHD deaths and cases which would theoretically be eliminated if 
smoking prevalence were reduced to zero. These estimates are conservative 
in that they assume that no other risk factors would change in a favorable 
direction. The CDC-based smoking prevalence data used in these 
calculations are in Tables S-2 and S-5. In general, the population 
attributable risk estimates (8, Table 17) closely parallel the prevalence 
data and to that extent show a high black-white ratio only among men over 
age 65, for whom the CDC data show a questionably high prevalence rate. 
For both white and black men between 25 and 65, smoking-related preventable 
CHD deaths are estimated at 33 to 37% of total CHD deaths. For CHD cases, 
percentages of preventable events are approximately 10% lower. A higher 
proportion of preventable black compared to white male CHD cases is 
suggested in the 45-64 year age-group as well as in men 65 years and over. 
(Note, the picture for smoking-related preventable cerebrovascular disease 
deaths is quite similar to that for CHD in this analysis, except that 
estimates of preventable cases among 45-64 men are the same for blacks and 
whites . ) 

Other "CHD impact" variables analyzed were proportional number of cases 
and deaths attributable to smoking, years of life lost, number of hospital 
and restricted activity days and medical costs which can be attributed to 
smoking. These estimates are summarized in Table S-7 for men. 



242 



Table S-7 Population attributable risk fractions for smoking 
for several CHD variables in non-white and white 
men: estimates for the U.S. population (8) 

Table No Variable Non-white White 

(percent of cases) 

23 CHD deaths 33 21 

24 CHD-related lost yrs . of life 35 34 

25 CHD cases 28 17 

26 CHD-related hospital days 27 16 

27 CHD-related days of rest, activ. 28 17 

28 CHD-related medical expend. 27 16 



All of these estimates show a proportionately greater impact on CHD of 
smoking in non-white compared to white men, with the exception of years of 
life lost. 

Estimates of the percent of CHD deaths in women that would be 
prevented if smoking in women were eliminated show a much lesser impact 
than in men, but very similar within-age percentages in black and white 
women: BW - 8.2, 6.7, and 3.7 % in the 25-44, 45-64 and 65+ age-groups, 
respectively; 8.8, 8.3, and 3.1% in white women. Referring back to the CDC 
prevalence data in Table S-5, the impact of smoking elimination in women is 
about a third of the prevalence of smoking, whereas in men the impact was 
approximately equal to the smoking prevalence. Data for women for the 
other CHD variables are summarized in Table S-8. Smoking attributable CHD 
risks in women are much lower than those for men and there are no racial 
differences. As pointed out in the Carter Center report, the impact is 
least for deaths and higher for variables which reflect the relatively 
young age of occurrence of smoking related CHD deaths and cases. 



Table S-8. Population attributable risk fractions for smoking 
for several CHD variables in non-white and white 
women: estimates for the U.S. population (8) 

"Table No Variable ' Non-white White 

(percent of cases) 

23 CHD deaths 4 4 

24 CHD-related lost yrs. of life 7 8 

25 CHD cases 12 10 

26 CHD-related hospital days 10 9 

27 CHD-related days of rest, activ. 12 10 

28 CHD-related medical expend. 10 10 



243 



Confidence in the estimates for the 65+ age male population is limited 
by the departure of smoking prevalence figures in black men from the 
pattern usually seen in the 65+ age-group. In men 25-64, based on data 
indicating roughly equivalent smoking prevalence in black and white men, 
the theoretical benefits of eliminating smoking in blacks are substantial. 
The population impact of smoking on CHD morbidity and mortality in black 
men may be slightly greater than for white men in the 45-64 age-group. 

Smoking has a lesser impact on CHD in women compared to men. When 
risks associated with smoking alone are considered, CHD impact is not 
different in black compared to white women. However, smoking enhances a 
more unfavorable multivariate risk picture for blacks than for whites. 

1.3 Implications 

That the basic association between smoking and CHD holds for blacks as 
well as whites is apparent from the studies available, although the degree 
of risk appears to be somewhat less in black compared to white men, and 
similar in black and white women. 

The dynamic state of population smoking behaviors over time and the 
substantial changes in IHD risk that occur with smoking cessation severely 
limit the utility of cross-sectional data. In addition, the sampling 
approach once appropriate to descriptions of the U.S. population is 
outdated. Since race has been recognized as an important proxy health 
variable, sampling approaches should be designed to permit racial subgroup 
comparisons as well as descriptions of U.S. population parameters in the 
aggregate. Such sampling should include awareness of the need to partition 
race and socioeconomic status effects . 

For example, the extent of socioeconomic differences among blacks is 
demonstrated in the hospitalized cancer control data from the American 
Health Foundation (11): both high school and college educated black men 
smoked more than white men, in both time periods studied (see Table S-1). 
However, the decrease in smoking prevalence among college educated black 
men was more than three times that in high school educated black men and 
nearly 60% greater than that in college educated white. Data aggregated on 
either educational level or race would not convey this difference, but the 
difference has important implications for intervention and provides 
important clues to patterns which might be hidden in longitudinal data 
which classify blacks and whites only on smoking status at entry. 

The longitudinal data available are outdated in terms of the current 
smoking prevalence and, as implied above, in terms of the actual smoking 
status of persons initially classified as smokers during the year or months 
immediately prior to fatal or morbid events. 

Consideration of potential benefits of intervening on smoking in black 
men and women should include the relative likelihood of success per unit of 
effort compared to the other risk reduction possibilities. Only minimal 
literature was identified relating to perspectives for intervention on 
smoking in the black population. NCHS data indicate that in 1978, black 



244 



men and women, although lighter smokers, are more likely to smoke 
cigarettes with high tar and nicotine content, that fewer blacks are 
successful when they attempt to stop smoking although more blacks had tried 
to quit at some time (2) . Sex difference in attempts to stop smoking were 
more pronounced in blacks than whites. Similar percentages of men and 
women had stopped smoking or attempting to in the year prior to interview 
(28.5 and 31.5%). Among black men and women, substantially more women than 
men had attempted to quit (44.2% vs. 34.1%). 

In the MRFIT randomized trial, thiocyanate-adjusted percentages of 
black and white men in the special intervention group who had stopped 
smoking at each annual visit were quite similar (13, Table 8). It is 
interesting to note that the unadjusted percentages among the black men 
were 6 to 15% higher than those of whites before adjustment, implying that 
reporting bias may have been greater in the black men. However, the 
success at smoking cessation in the special intervention group of black men 
was equal to that of whites (35.9 and 35.5 of white and black special 
intervention men stopped smoking) . Both blacks and whites in the usual 
care group were less successful in smoking cessation, and whites did 
somewhat better than blacks (22.2 vs. 18.9% stopped smoking). 

A study of factors influencing trial and adoption of smoking among 
children and adolescents (ages 8-17) in Bogalusa, Louisiana reported 
significant race and sex differences in the social learning which leads to 
eventual smoking (15). The number of "smoking models ' in the child s 
environment was found to predict whether a child would try smoking, but the 
pattern of influence was different in black compared to white children. 

1.4 Recommendation 

A broader base of short-range prevalence and trend data on smoking 
behaviors in blacks is needed, followed by specialized interventions to 
accomplish permanent smoking cessation in blacks. Although smoking 
cessation may be associated with some weight gain, there will still be a 
net benefit of the smoking cessation. Smoking differentials between blacks 
and whites do not parallel morbidity-mortality patterns. However, smoking 
is a risk factor for both CHD and for cancer. The need to reduce smoking 
prevalence among blacks should not be neglected. 



245 



1.5 References 

1. Bonham, GS. Use habits of cigarettes, coffee, aspirin, 
and sleeping pills. United States, 1976. Vital and health 
statistics. Series 10. Data from the National Health Survey; 
No. 131. DHEW Publication No. (PHS) 80-1559). October 

1979. 

2. Moss AJ. Changes in cigarette smoking and current smoking 
practices among adults. United States, 1978. National 
Center for Health Statistics. Advancedata. No. 52. September 
19, 1979. 

3. Kleinman JC, Feldman JJ, Monk MA. The effects of changes 
in smoking habits on coronary heart disease mortality. 

Am J Pub Health 1979;69:795-800. 

4. Schoenborn CA, Danchik KM. Health practices among adults, 
United States, 1977. National Center for Health Statistics. 
Advancedata No. 64. November 4, 1980. 

5. National Center for Health Statistics. Health United States 
1980, Tables 27 (pp 162-63) and 28 (pp 164-65). DHHS Pub. No. 
(PHS) 81-1232. Public Health Service. Washington. 

U.S. Government Printing Office, Dec. 1980. 

6. National Center for Health Statistics. Health United States, 
1983, Tables 30 (pp. 129-130) and 31 (pp. 131-132). DHHS 
Pub. No. (PHS) 84-1232. Public Health Service. Washington. 
U.S. Government Printing Office, Dec. 1983. 

7. Rowland MB, Fullwood R. Coronary heart disease risk 

factor trends in blacks between the first and second National 
Health and Nutrition Examination Surveys, United States, 
1971-1980. Am Heart J 1984;108:771-778. 

7a. Rowland M, Fulwood R, Kleinman JC. Changes in heart disease 
risk factors, in reference 7, pp. 13-17. 

8. Haynes SG, White CC, Tolsma D, Newman JM, McGee D. Closing 
the gap for cardiovascular disease. Carter Center Report 
August 27, 1984 (unpublished manuscript courtesy of Dr. Haynes) 
Table 16. 

9. Bradstock MK, Marks JS, Forman M, Gentry EM, Hagelin GC, 
Trowbridge FL. Behavioral risk factor surveillance. 1981-83. 
MMWR 1984;33: lss-4ss . (reference on methodology of CDC Survey) 

10. Garfinkel L. Cigarette smoking and coronary heart disease 
in blacks. Comparison to whites in a prospective study. 
Am Heart J 1984;108:802-806. 



246 



11. Covey LS, Mushinski MH, Wynder EL. Smoking habits in a 
hospitalized population. Am J Pub Health 1983;73:1293-1297. 

12. Neaton JD, Kuller LH, Wentworth D, Borhani NO. Total and 
cardiovascular mortality in relation to cigarette smoking, 
serum cholesterol concentration, and diastolic blood pressure 
among black and white males followed up for five years. 

Am Heart J; 1984; 108 : 759-770. 

13. Connett JE, Stamler J. Responses of black and white men 
to the special intervention program of the Multiple Risk 
Factor Intervention Trial (MRFIT) Am Heart J 1984; 108: 
839-850. 

14. Hypertension Detection and Follow-up Program. Baseline 
characteristics of the enumerated, screened, and hypertensive 
participants. The Hypertension Detection and Fol low-Up 
Program Cooperative Group. Hypertension 1983;5:IV-1 - IV-295, 

15. Hunter SM, Baugh JG, Webber LS, Sklov MC, Berenson GS . 
Social learning effects on trial and adoption of cigarette 
smoking in children. The Bogalusa Heart Study. Prev. Med. 
1982;11:29-42. 



247 



2 . CHOLESTEROL 

2. 1 Data sources 

The adequacy of the available data on cholesterol levels in black men 
and women is markedly influenced by the increasing interest in lipoprotein 
cholesterol components rather than total cholesterol. In particular, 
high-density lipoprotein cholesterol has been the focus of considerable 
recent interest both as a possible protective factor against IHD and as one 
for which black persons may have an advantage relative to their white 
age-sex peers (1-4). 

For total cholesterol, the Health Examination Survey (NHES, 1960-62) 
and National Health and Nutrition Examination Survey (NHANES I 1971-74 and 
NHANES II 1976-80) provide national probability estimates of distributions 
and means by age, sex, and race for black and white children and adults 
(5-7,9). Analyses of 1971-74 serum cholesterol levels by socioeconomic 
characteristics have also been published (8) . The NHES and NHANES data 
provide representative estimates of mean serum cholesterol levels and the 
prevalence of elevated cholesterol (using arbitrary cut points) for the 
time periods they cover and can, to some extent, be used to evaluate 
changes in the cholesterol levels of blacks and whites over time. 

Cycle II of the National Health and Nutrition Examination Survey will 
provide data on 1976-80 levels of high-density lipoprotein cholesterol 
(HDL) for a national probability sample of U.S. black and white men and 
women ages 20-74. Estimates of mean HDL levels for race-sex groups in 6 
age categories have been made. However, release of these data has been 
delayed due to a need to resolve methodological issues which influence 
interpretation of NHANES HDL values relative to published values from other 
large studies. These issues are currently being evaluated by the National 
Center for Health Statistics and the National Heart, Lung, and Blood 
Institute. 

For the purposes of this report to the Task Force on Black and Minority 
Health, Robert Murphy, Director of the NCHS Division of Health Examination 
Statistics, has authorized inclusion of certain provisional statements on 
black-white differences in mean HDL levels. These statements, included 
under "Findings" (section 2.2), were provided by Robinson Fulwood, Health 
Statistician (communication to Shiriki Kumanyika) , with certain caveats. 

Sample sizes for the NHANES II HDL values in blacks are small. Numbers of 
intended and actual HDL values in each age-group of black men and women are 
given in Table C-1. 



248 



Table C-1. Sample sizes for estimates of HDL values in black 
men and women ages 20-74, United States 1976-80. 





Black Men 




Age Group 


Intended" 


Actu 


20-24 


79 


65 


25-34 


139 


110 


35-44 


70 


53 


45-54 


62 


45 


55-64 


129 


91 


65-74 


128 


92 



Black 


Women 


Intended- 


■ Actual# 


94 


77 


145 


116 


103 


81 


100 


79 


135 


98 


152 


115 



Total 607 456 729 566 

" Intended = number of respondents for whom total cholesterol was determined 
# Actual = number of respondents for whom an adequate quantity of blood 

remained after determinations of total cholesterol and trigylcerides to 

permit determination of HDL-cholesterol as well 

For whites, HDL values are available for approximately 3800 men and 4300 
women. The smallest sample in any age-group for white men is 472 (581 
intended) ; for white women 506 (624 intended) . 



The sample sizes for blacks are adequate for stable estimation of mean 
HDL cholesterol levels in each sex-age-group according to the criteria 
applied by the Division of Health Examination Statistics. However, most of 
the age-sex samples of HDL values for blacks do not meet optimum criteria 
for estimation of standard errors. Thus tests of statistical significance 
of black-white differences must be interpreted cautiously. All of the 
sample sizes meet the criterion of a minimum of 25 for standard error 
estimation. However, only two of the groups (25-34 year-old black men and 
65-74 year-old black women) in the total cholesterol data (i.e., the 
numbers shown in Table C-1 as "intended") met a second criterion of having 
observations in both of the paired probability sampling units for at least 
12 of the 32 pseudostrata. ~ Since the first criterion is met in the HDL 
data, standard errors will be published, but with asterisks indicating that 
full confidence can not necessarily be placed in the starred standard error 
values or in related statistical tests. 

In this summary for the Task Force, emphasis has been given to 
published studies which present data comparing lipoprotein rather than only 
total cholesterol levels in blacks and whites, and primarily in the adult 
population at IHD risk. (If needed for reference, HDL comparisons in black 
and white neonates, preschool, school-age and adolescent children are 
summarized in a 1984 review by Glueck et al.(2)). Studies associating 
either total or HDL cholesterol with IHD risk have also been reviewed. 



249 



Data sources identified in addition to the NCHS population estimates 
can be categorized according to the relevant issues, as follows: 

a) comparisons of lipoprotein cholesterol levels in black 
and white men, women, or families (4,11-18); 

b) cholesterol comparisons between blacks and whites where 
the socioeconomic status of the black and white subjects 
is considered (4,11,13,14,17,19,33); 

c) studies related to possible explanations for HDL differences 

in blacks and whites, including data on lipoprotein cholesterol 
in Caribbean and African blacks (4,20-27); 

d) data comparing the effectiveness of dietary intervention 
on cholesterol levels in blacks and whites (28,29); 

e) estimates of the relative impact of. elevated serum cholesterol 
on IHD risk in blacks compared to whites (30-32) . 

The ascertainment of cholesterol levels is not equivalent across 
studies. Methodological differences include whether or not subjects had 
fasted before blood was drawn, whether cholesterol was measured in plasma 
or serum, whether samples were frozen before analysis and, if so, the time 
and conditions of storage, and analytic procedures. Although the effect of 
these factors on cholesterol determinations is not large, the small 
differences introduced complicate the interpretation of small differences 
in group means which, if real, may have important risk implications. Thus, 
comparisons across studies are made here only with reference to the 
relative consistency of racial differences observed in different data sets. 

2.2. Findings 

2.2.1 Total and lipoprotein cholesterol comparison among 
black and white men 

2.2.1.1 Total cholesterol: men 

Representative national data permitting comparisons of total 
cholesterol levels between black and white men within the three time 
periods of the NCHS examination surveys are shown in Table C-2. Data from 
the NHES are not strictly comparable with the NHANES data(6) . However, 
comparison of cholesterol distributions in NHANES I and II is appropriate 
for estimation of time trends. 



250 



Table C-2. Age-specific comparisons of mean serum cholesterol 
in national probability samples of U.S. black and 
white men in three time periods between 1960 and 
1980. 

NHES NHANES I NHANES II 

1960-62" 1971-75# 1976-80! 

( ragms per deciliter ) 

AGE BM WM BM WM BM WM 



25-34 


195.0 


207.1 


214.2 


209.9 






35-44 


217.2 


228.1 


224.7 


231.5 


207.1 


206.8 


45-54 


226.6 


231.4 


237.1 


239.9 






55-64 


229.5 


233.6 


243.8 


239.9 


227.8 


228.4 


65-74 


224.0 


229.9 


237.3 


236.4 


217.5 


221.8 


age 


210.5 


218.8** 


225.7 


217.5! ! 


215.4 


216.7! ! 


adjusted 















•'- Ref 5, Table 6 

** for ages 18-74; age-adjusted estimates not published for 

25-74 year-old adults 
# age-specific data for 1971-74, from ref 6, table 4 
! ref 30, table 15a; data for ages <65 grouped by 20 year spans 
!! age-adjusted data for 25-74 year-olds taken from ref 9, table VI 



In 1960-62, age-specific and overall serum cholesterol levels of black 
men were consistently less than those of white men. Age-specific data for 
1971-75 and 1976-80 do not show consistent black-white differences: The 
data in Table C-3 indicate a decrease in the prevalence of elevated serum 
cholesterol in black men between 1971-75 and 1976-80 but this decrease was 
not statistically significant. The prevalence of elevated serum cholesterol 
was eight percent higher in black than white men in 1971-75, decreased to 
3/0 higher in 1976-80. The largest decrease in cholesterol levels among 
black men was among men 55 or older. 



251 



Table C-3. Prevalence of Serum Cholesterol >260 mg/dl in 
black and white men, 1971-75 and 1976-80: age 
specific rates for black men ages 25-74; age- 
adjusted rates for black and white men ages 25-74. 



NHANES 1 19 71-75 



NHANES 11 1976-80 



AGE 



rate per 100 population 
Black Men 



25-34'' 

35-44 

45-54 

55-64 

65-74 



10.9 
24.3 
28.7 
32.3 
28.0 



9.3 
23.6 
25.3 
24.2 
18.7 



25-74# 



BM:23.2 WM:15.3 



BM: 19.3 WM:16.3 



" Ref 9, Table IV 



# Ref 9, Table V 



A consistent socioeconomic influence on cholesterol in black men has 
not been reported. An NCHS analysis of cholesterol levels in 1971-74 (8) 
suggests that the impression of socioeconomic effects is related to the SES 
variable used. Cholesterol levels in men tended to increase with 
increasing levels of annual family income. An inverse effect of education 
on serum cholesterol levels was observed in white but not black men. 

A discrepancy in SES effects on cholesterol in black and white men was 
observed in a MRFIT screenee population in California (33) . The prevalence 
of elevated cholesterol (defined as >= 260 mg/dl) among white men was lower 
at higher SES levels, using categories of a 77 point education-occupation 
scale as the SES measure. Cholesterol levels of the black screenees were 
different at different SES levels, but the direction of these differences 
was not consistent (33) . There were noteworthy black-white differences in 
the prevalence of elevated serum cholesterol in two of the six SES 
categories (lowest and second highest categories; prevalence higher in 
whites in both groups) . Prevalence rates in the other categories were 
similar (33, Table 3). The pattern seen may have been somewhat affected by 
differing distributions of the black and white men within the 35-57 year 
age range (52% of black men vs. 61% of white men were 45-57 years old). 

Total cholesterol levels of the black men in the Framingham Minority 
Study population were lower than those of the white men in every age-group 
studied (age range 20-69) and the age-adjusted means in black and white men 
were significantly different (11) . In this sample, 56% of black compared 
to 44% of white men under age 50 were college-educated. Sixty-four percent 
of black compared to 22% of white men over age 50 were college-educated. 



252 



2.2.1.2 Lipoprotein cholesterol: men 

HDL levels are consistently higher in black men than in white men in the 
20-74 year-old cross-section of NHANES II respondents. The size of the 
differences is relatively similar in the age-groups between 20 and 54 
(7, 6, 8, and 6 mg/dl in each successive age-group). Levels in white men are 
the same at ages 55-64 and 65-74, but levels in black men are higher in the 
55-64 year-olds than in younger or older black men. Thus the black-white 
difference is highest in the 55-64 year age-group (10 mg per dl) . The 
difference in 65-74 year-old men is 6 mg/dl, similar to that seen before 
age 55. The statistical significance of these differences has not yet been 
tested. The relationship of the HDL distributions to the respective total 
cholesterol distributions should be considered in interpreting these HDL 
data. 

As summarized by Glueck et al. (2), studies in black and white male 
children and adults suggest that HDL levels in black males are higher than 
those of whites from early childhood on and that the size of the difference 
increases after maturation. Maturational changes in lipid profiles occur 
in males of both races (decline in HDL, increases in low-density 
lipoprotein (LDL) cholesterol and triglycerides) but appear to follow a 
less atherogenic course in black vs. white males. 

The Evans County Heart Study investigators compared HDL and LDL 
cholesterol levels of 110 randomly-selected black men with those of white 
men individually matched on age and total cholesterol level (17). Men with 
evidence of CHD were excluded. With total cholesterol levels held constant 
(by matching) mean HDL cholesterol levels were significantly higher in the 
black men (by 11 mg/dl) and LDL cholesterol levels significantly lower (by 
6 mg/dl). The differences were not statistically explained by occupation, 
education, social class, or smoking habits but were to some extent 
explained by body mass differences between the black and white men. 
Consistency of these differences across age cannot be determined due to the 
age-matching analytical approach. HDL and LDL cholesterol levels of black 
and white men in the upper tertile of the Quetelet index were not different 
(17, Figure 8) . 

More recent studies in the Evans County population further specify 
apolipoprotein differences between black and white men (4). Apo A-1 levels 
were significantly higher and Apo C-II significantly lower in black than 
in white men, suggesting that -black men in Evans County have a greater 
proportion of the (lighter, cholesterol-rich) HDL-2 subfraction. Alcohol 
consumption rather than race was a significant variable in levels of Apo 
A-II. The differences in levels of Apo C-II but not Apo A-I were still 
statistically significant after adjustment for age, Quetelet index, 
smoking, and alcohol consumption. 

The Lipid Research Clinics (LRC) Program has contributed several studies 
which consistently indicate a more favorable lipid profile in black 
compared to white men (the LRC protocol excludes men using antidiabetic, 
antiuricemic, antihypertensive, or lipid lowering medications). The 
Cincinnati LRC Population Study compared lipoprotein cholesterol levels of 



253 



43 pairs of black and white men, ages 20 to 60, matched on age and total 
plasma cholesterol. HDL levels were significantly higher and LDL/HDL 
ratios significantly lower in black men (15). A substudy in 9 pairs of 
hypercholesterolemic men (total plasma cholesterol >250 mg/dl) yielded the 
same results (15). 

The Princeton School District Study of the Cincinnati LRC compared HDL 
and LDL levels in black and white men ages 20-59. This study also 
indicated significant racial differences (higher HDL and lower LDL in black 
men) (12). Age-group (20-39 or 40-59) did not affect relative HDL and LDL 
levels, although total plasma cholesterol was higher in the older men. A 
study of socioeconomic factors and CHD risk in the same population 
indicated that HDL and LDL differences between blacks and whites remain 
after adjustment for education and occupation (13). 

Black-white differences in cholesterol in men age 20-44 years were 
analyzed in pooled screening data from five LRC centers (14). Higher HDL 
and lower LDL were observed for black men when the distributions of these 
variables were compared by pooling across age with covariance adjustment 
for age, total cholesterol, and Quetelet Index. Similar differences were 
observed when comparisons were made between pairs of black and white men 
matched for age and total cholesterol. Stepwise covariance adjustment for 
possible confounding factors indicated that with age and total cholesterol 
effects statistically removed, Quetelet index had a small negative 
confounding effect on black-white differences in HDL-cholesterol levels 
(i.e., the difference increased from 8.3 to 9.5 mg/dl when Quetelet index 
was added as a covariate) . Triglycerides had a positive confounding effect 
(the difference decreased from 9.5 to 7.9 mg/dl with the further addition 
of triglycerides to the equation) . 

In a collaborative LRC report combining data on men ages 20-79 from 
ten study centers, a greater proportion (17% vs. 3%) of black men than 
white men with high total cholesterol were of the hyperalpha type (16). 
This was found using either of two definitions of hypercholesterolemia 
(race-age-sex specific 95th percentile or an age-specific cut point) . 

Although the reported black-white differences in HDL and LDL levels 
were not statistically explained by socioeconomic status variables in the 
above studies, the limited range of socioeconomic status among black 
subjects may give an incomplete picture on this point. Black men in the 
Evans County cohort were of low socioeconomic status whereas the white 
subjects include both low and high SES persons (32). In the Cincinnati 
Princeton School District Study (13), some black households were in the 
highest education and income categories but the numbers of these were too 
small to permit stratum specific comparisons. Thus, although an overall 
black-white difference may still remain after differences in the 
black-white SES distribution have been accounted for, it is not certain 
that the high SES black men have the advantageous lipid profiles relative 
to their white counterparts . 



254 



The Framingham Minority Study (11) is unique in having compared blacks 
and whites in a sample which included a high proportion of college-educated 
black men. HDL-cholesterol levels of black men in this study were not 
higher than those of the white men. In fact, the mean HDL levels of the 
black men were significantly lower than those of the white men, although 
the ratio of mean HDL cholesterol to mean total cholesterol (which was also 
significantly lower in black men) was similar. 

The Framinghman Minority Study finding is supported by a report from 
the Bogalusa study. Hunter and coworkers reported that although 
alpha- lipoprotein levels of black children were higher and beta- lipoprotein 
levels lower than those of white children in most parental -education 
categories, an opposite pattern was observed among children whose parents 
had a post-graduate education (19). When the parental SES variable was 
blue vs. white collar occupation, black children but not white children had 
SES-related differences in mean alpha- lipoprotein levels. Racial 
differences in alpha- lipoprotein levels decreased from 64 mg/dl (black 
children higher) among children of blue collar workers to only 6.9 mg/dl 
(black children higher) among children of white collar workers. The 
relative difference in alpha-lipoprotein levels between children of blue 
vs. white collar parents was much larger than that for total cholesterol, 
beta- or pre-beta-lipoprotein levels. 

In summary, when one assesses differences in total cholesterol between 
blacks and whites, HDL-cholesterol levels should be considered. The total 
cholesterol/HDL cholesterol ratio is needed for useful HDL comparisons in 
data where subjects have not been matched on cholesterol levels or HDL 
levels. Significant declines in the prevalence of elevated serum 
cholesterol levels are not evident in the NHANES data for either black or 
white men. Socioeconomic aspects of cholesterol-related risk may vary 
with the indicator used, are probably different for black and white men, 
and are not monotonic in black men. More data are needed on this point. 
With the exception of a study which included a large percentage of high SES 
black men, higher HDL cholesterol levels in black compared to white men are 
a consistent finding, across several studies and at several ages. 
Apparently, the protection theoretically afforded by HDL cholesterol does 
not effectively counter other risk factors in black men under age 60 years, 
since prevalence/ incidence of IHD appears similar in younger black and 
white men. 



2.2.2. Total and lipoprotein cholesterol comparisons among 
black and white women. 

2.2.2.1 Total cholesterol: women 

National probability estimates of mean serum cholesterol and 
elevated serum cholesterol in black and white women in the United 
States are shown in Tables C-4 and C-5. In 1960-62, overall mean 
cholesterol levels of black women were lower than those of white 
women. Levels of black and white women tended to diverge with 
increasing age, with the largest difference in women 55-64. For 
NHANES I, the age-specific data indicate slightly higher cholesterol 



255 



levels in black vs. white women under age 65, although the overall 
age -adjusted means for the two racial groups are identical. 
Cholesterol levels of black and white women changed only slightly 
between 1971-75 and 1976-80. Black women aged 45-64 years had 
slightly lower mean levels than white women. 



Table C-4. Age-specific comparisons of mean serum cholesterol 
in national probability samples of U.S. black and 
white women in three time periods between 1960 and 
1980. 

NHES NHANES I NHANES II 

1960-62* 1971-75# 1976-80! 



milligrams per deciliter 



AGE 


BF 


WF 


BF 


WF 


BF 


WF 


25-34 


197.9 


198.0 


207.3 


202.8 






35-44 


213.1 


214.2 


216.9 


216.4 


198.3 


198.3 


45-54 


232.2 


237.6 


244.7 


242.5 






55-64 


239.0 


264.9 


260.8 


256.4 


237.8 


239.7 


65-74 


258.2 


267.4 


259.7 


261.8 


242.6 


246.3 


age 


217.8 


224 . 1** 


221.2 


221.4!! 


219.2 


219.9! ! 


adjusted 















* Ref 5, Table 6 

"" for ages 18-74; age-adjusted estimates not published for 

25-74 year-old adults 
// age-specific data for 1971-74, from Ref 6, Table 5 
! Ref 30, Table 15b; data for ages <65 grouped by 20 year spans 
!! age-adjusted data for 25-74 year-olds taken from Ref 9, Table VI 



Table C-5 indicates inconsistent trends in the prevalence of 
elevated serum cholesterol (using a 260 mg/dl cut point) among 
different age-groups of black women between NHANES I and NHANES II. 
The largest change was a decrease among the oldest group of women; 
however, prevalence rates for women age 35-64 years increased 
slightly. The similarity of age-adjusted rates for black women in 
NHANES I and NHANES II may be misleading because age adjustment 
obscures age-specific trends. 



256 



Table C-5. Prevalence of Serum Cholesterol >260 mg/dl in 

black and white women, 1971-75 and 1976-80: age 
specific rates for black women aged 25-74; age- 
adjusted rates for black and white women aged 
25-74. 

NHANES I 1971-75 NHANES II 1976-80 

rate per 100 population 
AGE Black Women 

25-34" 8.7 6.0 

35-44 7.7 13.3 

45-54 23.5 25.0 

55-64 29.3 32.2 

65-74 43.5 29.9 

25-74# BF:19.6 WF:20.2 BF: 19.0 WM:19.5 

''•Ref 9, Table IV # Ref 9, Table V 



The NCHS analysis of socioeconomic influences on serum cholesterol 
levels of NHANES I adult female respondents indicated an inverse effect of 
both education and income (8) . This inverse effect in women was in 
contrast to the weakly positive effect observed in men. The income effect 
was significant in white but not black women. In the Framingham Minority 
Study (11), total cholesterol levels of the black women were lower than 
those for white women for all age-groups studied (range 20-69) except women 
aged 50 to 59 years. Sixty-five percent of the black vs. 32% of the white 
women under age 50 years in the Framingham Minority Study sample were 
college-educated. Among the women over age 50, 27% of the black vs. 14% of 
the white women were college-educated. 

2.2.2.2 Lipoprotein cholesterol: women 

In the NHANES II data, high-density lipoprotein cholesterol levels are 
consistently higher in black women than in white women although the 
differences are smaller than those seen in men. As in men, the largest 
black-white difference in HDL levels among women is in the 55-64 year age 
group. Differences between ages 20 and 54 are 4, 2, 3, and 1 mg/dl in 
successive age-groups. In the 55-64 year-old women, HDL levels are 6 mg/dl 
higher in black women than white women, due primarily to an increase in the 
black women. HDL levels are somewhat lower for both black and white women 
in the 65-74 year-old age-group, but the black-white difference decreases 
to 4 mg/dl due to a larger drop in the HDL levels of the black women. 

Thus, black-white differences in lipoprotein cholesterol for women 
parallel those for men but are of a lesser magnitude. This parallel 
picture of slightly, but not substantially higher HDL and lower LDL levels 
among black compared to white women is reported in several studies 



257 



described earlier for men (12,14-17). In the Cincinnati LRC Princeton 
School Study, HDL differences in black compared to white women were larger 
in women not using exogenous sex steroid hormones than in women who were 
using them and were statistically significant in the nonhormone using 
group (12). In the collaborative LRC Prevalence Study, the increase in 
age- total cholesterol-adjusted HDL differences in black and white women 
when the Quetelet index was added to the equation was greater than the 
increase in men. When the Quetelet index was in the model, the higher mean 
HDL cholesterol levels in black women were statistically significant 
(further addition of trigylcerides decreased the difference to 
nonsignificant levels) (14). 

HDL-cholesterol differences in women in the Framingham Minority Study 
also parallel those in men, i.e., HDL and total cholesterol levels in black 
women were significantly lower than in white women (with the exception of 
higher total cholesterol levels in black than in white women age 50-59). 
However, HDL/total cholesterol ratios were similar in black and white 
women. The mean Quetelet index of black and white women in this sample was 
not different. 

In summary, distributions of serum cholesterol and lipoprotein cholesterol 
are similar in black and white women. Data regarding socioeconomic 
influences on cholesterol in women are limited. NHANES I data suggest that 
levels of cholesterol increase as SES decreases. If so, then the larger 
proportion of black than white women who are of low SES are at risk for 
elevated cholesterol. Black-white differences in levels of HDL cholesterol 
which would be expected on the basis of findings in men are suggested in 
the data for women but are usually very small and not significant. When 
the entire adult age spectrum is considered, serum cholesterol levels 
appear to have remained stable in both black and white women between 
1971-75 and 1976-80. However, a higher prevalence of elevated cholesterol 
in 35-64 year-old black women in NHANES II compared to NHANES I is 
suggested by the data. This may be a noteworthy finding, if valid. Any 
trends towards increased risk in black women should be targeted for 
intervention, due to the excess of other risk factors and IHD prevalence in 
this group. 

2.2.3 Basis of lipoprotein cholesterol differences in blacks 
and whites 

Gartside et al. (22) examined the extent and direction of black-white 
differences in several factors associated with HDL-levels including: 
intakes of protein, fat, carbohydrate, saturated fat, oleic acid, lineoleic 
acid and cholesterol (total and per kilogram of body weight) ; Quetelet 
index, self -reported maximum and minimum weight and weight at age 25; 
alcohol intake; cigarette smoking,; leisure time exercise and habitual 
physical activity; self -reported prevalence of diabetes; and hypertension. 

Of the factors found to differ between blacks and whites in NHANES II, 
the substantially higher relative weight of black compared to white women 
appeared to be the most likely explanation for the loss of the HDL 
advantage for black women. Substantial differences in obesity between 



258 



black and white men were not evident in the national population data and 
most of the studies reviewed. The greater prevalence of diabetes and the 
greater tendency to be treated with HDL- lowering antihypertensive 
medications among blacks than whites would work in the same direction for 
women. Higher levels of habitual activity in black than in white men at 
some ages would tend to enhance differences (22) . 

As noted above, adjustment for the Quetelet index has been more often 
reported to alter the observed black-white differences in HDL-cholesterol 
than does controlling for other possible confounders (14,17). The 
environmental influence on lipoprotein patterns is also suggested by the 
absence of significant black-white differences at birth (2) and by a 
possible disappearance of racial differences among high SES groups. 

It might be said that a genetic basis for lipoprotein profile 
differences between blacks and whites is suggested by studies of blacks in 
other countries. For example, in a study of men from 13 countries, the 
highest HDL to total cholesterol ratios were observed among African men 
(21). In his review of CHD in developing countries, Watkins cites several 
studies indicating that lipoprotein profiles among African and Caribbean 
men are favorable to low CHD risk (20) . These findings clearly do not 
separate genetic from environmental influences on differential lipid 
patterns . 

Gartside et al. postulate that genetic selection has favored blacks 
with relatively higher HDL related to the protective role of 
HDL-cholesterol against sleeping sickness (22). In this respect, it is 
also interesting to note a recent report by Dai et al. of a possible direct 
or indirect positive association between HDL levels and plasma testosterone 
in a sample of 255 MRFIT participants (23). Studies by Ross et al. have 
postulated that higher testosterone levels in black men might explain their 
higher prevalence of prostatic cancer compared to white men (24) . 

2.2.4 Impact of cholesterol-associated risk on CHD disparities 
between blacks and whites 

The importance of black-white differences in lipoprotein profiles 
may be much more in the utility of racial contrasts for etiologic analyses 
than in the potential for reducing racial disparities in CHD incidence and 
prevalence. The Cincinnati LRC group concluded (based on familial 
aggregation studies) that the relative contribution of genetic compared to 
environmental factors to HDL levels may be greater in blacks than whites 
(2). This line of reasoning is compatible with the lesser consistency and 
strength of association between lipid levels and measures of obesity in 
black compared to white children (25) and adults (26) and with lesser 
effects of cigarette smoking and oral contraceptives on HDL in black 
compared to white children and adolescents (27) . This might suggest that 
interventions directed specifically at the HDL component of cholesterol 
would yield a relatively lesser benefit for blacks. This is a testable 
hypothesis . 



259 



Berenson and coworkers have pointed out that the proneness of blacks 
to other CHD risk factors may override the degree of "subtle protection" 
afforded by high alpha-lipoprotein levels (25). Considering that the 
overall lipid picture is better for black men and no worse for black women 
compared to their age-sex peers, the similar rates of CHD in black men 
compared to white men before age 55 or 60 and in black women at all ages 
indirectly supports this conclusion. Analyses in the Cooperative 
Lipoprotein Phenotyping Study indicate that HDL levels were lower in CHD 
cases compared to control in black, white and Japanese men (18). However, 
a tabulation of CHD prevalence rates by HDL cholesterol level implied a 
threshold effect rather than a gradient. Prevalence rates did not differ 
markedly among men with HDL-cholesterol levels between 45 and 75 mg/dl. 
The striking prevalence differences were between men with HDL cholesterol 
levels less than 35 or 25 mg/dl (18) . The HDL levels in most of the 
studies of black-white differences report mean cholesterols in the 
intermediate rather than low range, possibly because persons at highest 
risk have been excluded by the study protocols. 

However, this does not advise against efforts to prevent or reverse 
trends toward elevated total cholesterol in the black population. The 
NHANES data suggest that the prevalence of elevated serum cholesterol in 
black men may be higher than that of white men (Table C-3) using 260 mg/dl 
as a cut point. The impression from multivariate analyses is that, with 
other factors held constant, the impact of elevated serum cholesterol on 
CHD in blacks is not substantially different from that in whites (31,32). 
In addition, when higher prevalence of hypertension and smoking (black men) 
are factored in, any added risk factor multiplies the risk of IHD. 

The Carter Center findings on the potential benefits of reducing serum 
cholesterol levels in the population can be summarized as follows (see 
section 1.2.1 (data sources on the impact of smoking on IHD risk) for a 
description of the Carter Center analytic approach) . 

In men, the proportion of CHD deaths that could be prevented if 
borderline (240-259 mg/dl) and elevated (>= 260 mg/dl) cholesterol levels 
were decreased to 219 mg/dl (considered to be normal) is slightly greater 
for black than white men (14.1 vs. 9.0 percent) in the 25-44 year age 
range. The comparable proportions for black and white men ages 45-64 and 
65 plus are approximately eight and three percent, respectively, in both 
racial groups. Proportionate reductions in CHD cases are 11 and 7% for 
black and white men ages 25-44, 12 and 10 percent for 45-64 year-old men 
and 8% in black and white men ages 65 and over (30) . 

In women, the greatest reductions in CHD mortality associated with 
reduction of borderline and elevated cholesterol levels to below 220 mg/dl 
would be among women over age 45, approximately 18% in both black and white 
women. Below age 45, reduction in CHD deaths among women is a third of 
that after age 45 and is the same (6%) for black and white women. The 
potential benefits of such cholesterol reductions on CHD cases among women 
is more striking: 18% among women under age 45 and 38-39% among women over 
age 45, again, with the same level of benefit in women of both races (30) 



260 



The Carter Center report (30) also presents estimates for the 
theoretical possibility of reducing cholesterol levels above 260 mg/dl to 
below that level. Percentage reductions follow similar patterns as those 
described above, but are much lower. For example, reductions in CHD cases 
among women over age 45 would be 18-22 percent compared to the 38-39 
percent which would occur if "normal" were defined as below 220 mg/dl. 

Carter Center population attributable risk fractions for cholesterol 
on CHD are summarized in Table C-6 for non-white and white men and women. 
The earlier stated pattern of greater potential benefits in women but with 
no substantial racial difference is also reflected in these estimates. 



Table C-6. Population attributable risk fractions for cholesterol 
on several CHD variables in non-white and white men and women: 
estimates for the U.S. population (30) 



Table 


CHD 




MEN 






WOMEN 




No* 


Variable 


Non-white 


White 


Non-white 


White 










(percent 


of 


cases) 




23 


deaths 


5 




5 1 




17 


19 


24 


yrs.lost life 


10 




8 1 




15 


16 


25 


cases 


11 




9 1 




35 


38 


26 


hospital days 


10 




9 1 




37 


38 


27 


restrict, act. 


11 




9 1 




35 


38 


28 


medical expend. 


11 




9 1 




38 


38 



in Reference 30 



2.2.5 Intervention Studies 

The limited evidence identified on the effectiveness of dietary ■ 
intervention on cholesterol levels of hyperlipidemic black women and men is 
quite encouraging. A report from the Chicago Heart Association (29) 
indicated that an educational intervention was more successful with black 
men and women than with whites. Most of the participants in this study 
were black, primarily from the inner city. Six to nine months after entry 
into the program, the black participants, who had higher cholesterol levels 
at baseline, had made slightly greater changes in fat consumption and had 
achieved greater reductions in cholesterol levels (8.1 vs. 4.5%, p<0.05) 
than white participants. The majority of participants (60%) were women; 
dietary adherence among women was better than among men. Nutritional 
knowledge scores of blacks were lower at baseline but were equivalent to 
those of whites after one, six, and nine months of intervention. In the 
MRFIT study, plasma cholesterol levels of black and white men decreased to 
a similar extent. Improvements of special intervention compared to usual 
care black men were slightly greater than for whites (28) . 



261 



2.3 Recommendation 

The evidence of equivalent or better lipoprotein profiles in blacks 
does not justify inattention to cholesterol levels in blacks. Efforts 
targeted to blacks should be included in the general effort to shift the 
distribution of cholesterol levels in the population downward. This should 
not, however, take priority over targeted interventions on hypertension, 
obesity, LVH, and smoking in blacks. 



262 



2.4 References 

1. Gillum RF, Grant CT. Coronary heart disease in black 
populations. II. Risk factors. Am Heart J; 1982: 104:852-864. 

2. Glueck CJ, Gartside P, Laskarzewski PM, Khoury P, Tyroler 
HA. High-density lipoprotein cholesterol in blacks and 
whites. Potential ramifications for coronary heart disease. 
Am Heart J. 1984;108:815-826. 

3. Curry CL, Oliver J, Mumtaz FB. Coronary artery disease 
in blacks. Risk factors. Am Heart J 1984;108:653-657. 

4. Heiss G, Schonfeld G, Johnson JL, Heyden S, Hames CG, 
Tyroler HA. Black-white differences in plasma levels of 
apolipoproteins . The Evans County Heart Study. Am Heart 
J 1984;108:807-814. 

5. National Center for Health Statistics. Serum cholesterol 
levels of adults. United States 1960-62. Vital and Health 
Statistics. PHS Publication No. 1000. Series 11. No. 22 
March 1967. Washington, D.C. 

6. National Center for Health Statistics. Total serum cholesterol 
levels of adults 18-74 years. United States 1971-74, by 
Sidney Abraham, Clifford Johnson, and Margaret Carroll. 

Vital and Health Statistics. Series 11, Data from the 
National Health Survey; No 205. DHEW Publication No. (PHS) 
78-1652. April 1978. 

7. National Center for Health Statistics. Total serum cholesterol 
levels of children 4-17 years, United States, 1971-74, 

by Sidney Abraham, Clifford Johnson, and Margaret Carroll. 
Vital and Health Statistics. Series 11. No. 207. DHEW 
Pub No. (PHS) 78-1655. 1978 

8. National Center for Health Statistics. Serum cholesterol 
levels of persons 4-74 years of age by socioeconomic charac- 
teristics. United States 1971-74, by Robinson Fulwood, 
Sidney Abraham, and Clifford Johnson. Vital and Health 
Statistics Series 11, No.- 217. DHEW Publication No. (PHS) 
80-1667. 

9. Rowland ML, Fulwood R. Coronary heart disease risk factor 
trends in blacks between the first and second National 
Health and Nutrition Examination Surveys, United States, 
1971-1980. Am Heart J 1984;108:771-779. 

10. Namboodiri KK, Green PP, Kaplan EB , Tyroler HA, Morrison 
JA, Chase GA, Elston RC , Rifkind BM, Glueck CJ. Familial 
aggregation of high density lipoprotein cholesterol. 

The Collaborative Lipid Research Clinics Program Family 
Study. Arteriosclerosis 1983;3:616-626. 



263 



11. Wilson PWF, Savage DD, Castelli WP, Garrison RJ, Donahue 

RP, Feinleib M. HDL-cholesterol in a sample of black adults. 
The Framingham Minority Study. Metabolism 1983;32:328-332. 

12. Morrison JA, Khoury P, Mellies M, Kelly K, Horvitz R, Glueck 
CJ. Lipid and lipoprotein distributions in black adults. 
The Cincinnati Lipid Research Clinics Princeton School 
Study. JAMA 1981;245:939-942. 

13. Khoury P, Morrison JA, Laskarzewski P, Kelly K, Mellies 

MJ, King P, Larsen R, Glueck CJ. Relationships of education 
and occupation to coronary heart disease risk factors in 
schoolchildren and adults. The Princeton School District 
Study. Am J Epidemiol 1981;113:378-395. 

14. Tyroler HA, Glueck CJ, Christensen B, Kwiterovich PO. 
Plasma high-density lipoprotein cholesterol comparisons 
in black and white populations. Circ 1980;62: IV-99 - 
IV-107. 

15. Morrison JA, de Groot 1, Kelly KA, Mellies MJ, Khoury P, 
Edwards BK, Lewis D, Lewis A, Fiorelli M, Heiss G, Tyroler 
HA, Gleuck CJ. Black-white differences in plasma lipids 
and lipoproteins in adults. The Cincinnati Lipid Research 
Clinic Population Study. Prev Med 1979;8:34-39. 

16. Morrison JA, Khoury P, Laskarzewski P, Gartside P, Moore 

M, Heiss G, Glueck CJ. Hyperalphalipoproteinemia in hyper- 
cholesterolemic adults and children. Trans Assoc Am Phys 
1980;93:230-243. 

17. Tyroler HA, Hames CG, Krishan 1, Heyden S, Cooper C, Cassell 
JC. Black-white differences in serum lipids and lipop- 
rotein in Evans County. Prev Med 1975;4:541-549. 

18. Castelli WP, Doyle JT, Gordon T, Hames CG, Hjortland MC, 
Hulley SB, Kagan A, Zukel WJ. HDL cholesterol and other 
lipids in coronary heart disease. The Cooperative Lipoprotein 
phenotyping study. Circ 1977;55:767-772. 

19. Hunter SM, Frerichs RR, Webber LS, Berenson GS. Social 
status and cardiovascular disease risk factor variables 

in children. The Bogalusa Heart Study. J Chron Dis 1979; 
32:441-449. 

20. Watkins LO. Coronary heart disease and coronary disease 

risk factors in black populations in underdeveloped countries. 
The case for primordial prevention. Am Heart J 1984; 108: 
850-862. 



264 



21. Knuiman JT, West CE, Burema J. Serum total and high density 
lipoprotein cholesterol concentration and body mass index 

in adult men from 13 countries. Am J Epidemiol 1982; 116: 
631-642. 

22. Gartside PS, Khoury P, Glueck CJ. Determinants of high-density 
lipoprotein cholesterol in blacks and whites. The second 
National Health and Nutrition Examination Survey. Am Heart 

J 1984;108:641-653 

23. Dai WS, Gutai JP, Kuller LH, Laporte RE, Falvo-Gerrard 

L, Caggiula A. Relation between plasma high-density lipoprotein 
cholesteroland sex hormone concentrations in men. Am J 
Cardiol 1984;53:1259-1263. 

24. Ross RK, Paganini-Hill A, Henderson BE. The etiology of 
prostate cancer. What does the epidemiology suggest? 
The Prostate 1983;4:333-343. 

25. Berenson GS, Webber LS, Srinivasan SR, Cresanta JL, Frank 
GC, Farris RP. Black-white contrasts as determinants 

of cardiovascular risk in childhood. Precursors of coronary 
artery and primary hypertensive disease. Am Heart J 
1984;108:672-683. 

26. Khoury P, Morrison JA, Mellies MJ, Gleuck CJ. Weight change 
since age 18 in 30-to-55-year-old whites and blacks. Assoc- 
iations with lipid values, lipoprotein levels, and blood 
pressure. JAMA 1983;250:3179-3187. 

27. Webber LS, Hunter SM, Baugh JG, Srinivasan Sr, Sklov 
MC, Berenson GS. The interaction of cigarette smoking, 
oral contraceptive use, and cardiovascular risk factor 
variables in children. The Bogalusa Heart Study. Am J 
Pub Health 1982;72:266-274. 

28. Connett JE, Stamler J^ Responses of black and white males 
to the special intervention program of the Multiple Risk 
Factor Intervention Trial. Am Heart J 1984;108:839-849. 

29. Mojonnier ML, Hall Y, Betkson DM, Robinson E, Wethers B, 
Pannbacker B, Moss D, Pardo E, Stamler J, Shekel le RB, 

Raynor W. Experience in changing food habits of hyperlipidemic 
men and women. J Am Dietet A 1980;77:140-148. 

30. Haynes SG, White CC, Tolsma D, Newman JM, McGee D. Closing 
the gap for cardiovascular disease. Carter Center Report. 
August 27, 1984. 



265 



31. Neaton JD, Kuller LH, Wentworth D, Borhani NO. Total 
and cardiovascular mortality in relation to cigarette 
smoking, serum cholesterol concentration, and diastolic 
blood pressure among black and white males followed up 
for five years. Am Heart J 1984;108:759-770. 

32. Tyroler HA, Knowles MG, Wing SB, Logue EE, Davis CE, Heiss G, Heyden 
S, Hames CG. Ischemic heart disease risk factors and twenty- 
year mortality in middle age Evans County black males. 

Am Heart J 1984;108:738-746. 

33. Kraus JF, Borhani NO, Franti CE . Socioeconomic status, 
ethnicity, and risk of coronary heart disease Am J Epidemiol 
1980;111:407-414. 



266 



3.0 ELEVATED BLOOD PRESSURE AND HYPERTENSION 

3.1 Prevalence 

3.1.1 Data Sources 

The NCHS Health Examination and Health and Nutrition Examination 
Surveys (NHES and NHANES) provide probability estimates for several blood 
pressure variables for black and white adults in the U.S. population for 
three time periods (1960-62, 1971-75, and 1976-80). Measurements and 
definitions in NHES and NHANES I and II are sufficiently comparable to 
permit valid estimates of trends in hypertension prevalence among blacks 
and whites over the 1960-1980 period. Several NCHS reports (1-4) have 
served as the basis for the following discussion of prevalence of elevated 
blood pressure and hypertension for race-sex groups in the age range 25-74 
years. When considering the black-white comparisons which follow, the 
larger standard errors of the estimates for blacks should be kept in mind. 

In addition, for 1971-75, published tables are available for estimates 
of blood pressure variables by geographic region, urban/rural residence and 
socioeconomic status. These data are of interest because of possible 
variation in hypertension patterns in blacks and whites in demographic 
sub-categories in the U.S. 

Emphasis has been given to variables for which tabulations for all 
three surveys are available by race and sex. These variables are as 
follows: elevated blood pressure, (defined by NCHS as systolic blood 
pressure (SBP) of at least 160 and/or diastolic blood pressure (DBP) of at 
least 95), hypertension (elevated blood pressure and/or on medication), 
previously undiagnosed hypertension, treated hypertension, and controlled 
hypertension. Although the cut points for designation of elevated blood 
pressure are somewhat arbitrary, the ones used by NCHS are useful for 
comparing NHES and NHANES data. There is no indication that different 
conclusions about black-white disparities would be drawn if variables 
reflecting the entire blood pressure distributions were to be used. 

NCHS blood pressure estimates reported here are based on three readings 
taken at specified points in the examination protocols (the NHANES I and 
NHANES II measurements each include one reading with the respondent supine; 
other readings were with respondents sitting) . Data for the different time 
periods have been age-adjusted, (by NCHS) to the U.S. population at the 
midpoint of NHANES II (1978) for comparison purposes. 

Now that substantial progress in blood pressure treatment and control 
among both blacks and whites has been documented, the changes in patterns 
of hypertension in blacks, compared to whites, over time deserve special 
attention (i.e., have there been decreases in the black-white disparities 
on hypertension variables?). Also, trends in the prevalences of target 
organ damage and hypertension-related end points deserve careful 
assessment . 



267 



Prevalence is a function of incidence and duration. That is, the 
percentage of people in the population who will be found to have 
hypertension at a given point in time is influenced both by the percentage 
of new cases of hypertension at that point (incidence) and by the 
percentage of people with hypertension who are surviving (duration) . If 
the rate at which new cases of hypertension develop remains constant, the 
proportion of hypertensives in the population will increase if 
hypertensives are effectively treated and thereby live for longer time 
periods. Effective treatment of hypertension should be reflected in a 
decrease in the prevalence of elevated blood pressure. However, the 
survival of hypertensives is not only a function of blood pressure level 
but also of the degree of end organ damage and comorbidity. These may 
differ among controlled hypertensives with similar blood pressures. For 
example, among hypertensive men in the Hypertension Detection and Follow-up 
Program randomized trial, black men had substantially higher mortality than 
white men (black-white ratios of 5-year-life table all-cause mortality were 
1.8 and 1.9 in stepped and referred care groups) (6). The variable which 
most differentiated the black and white men at baseline was prevalence of 
ECG-LVH. In addition, more of the black men were on antihypertensive 
medication at baseline and more had a history of diabetes or stroke (6) . 

The incidence of hypertension is difficult to ascertain. Long-term 
follow-up of large populations, with careful attention to the initial 
definitions of who is normotensive at the outset, are needed. Attempts to 
ascertain hypertension incidence among blacks have been summarized in a 
recent review by Oni (5). In cross-sectional data used for time trend 
analyses, incident and prevalent cases among the newly-identified 
hypertensives are difficult to separate on the basis of blood pressure 
measurement alone. Newly identified cases of elevated blood pressure may 
have been of longstanding duration. Patterns of hypertension incidence 
over time are essentialy unknown. 

At present, there is no basis for assuming that the incidence of 
hypertension has decreased, since the major efforts have been at the level 
of secondary, rather than primary prevention. These secondary prevention 
efforts are expected to prolong the lives of people with hypertension, 
i.e., to increase the duration of hypertension, and might be expected to 
result in increased prevalence over time. If similar or decreased 
prevalence is seen, then the possibility that treated hypertensives are 
dying at similar or greater rates should be considered. This could be due 
to increased case-fatality among hypertensives (perhaps associated with a 
particular type of treatment) , or to coincidental increases in overall 
mortality of persons with hypertension due to other causes. Another likely 
possibility is that hypertensives, especially mild hypertensives, may go 
off of medication after a long period of control and not have increases in 
blood pressure for several months. In a cross-sectional survey, such 
individuals would not be classified as hypertensive by either the elevated 
blood pressure or the "on medication" criteria. 



268 



3.1.2 Findings 

3.1.2.1 Elevated Blood Pressure and Hypertension in Black and 
White Men, 1960-1980 

Prevalence rates of elevated blood pressure for black and white men in 
1976-80 (the most current national probability sample estimates available) 
are compared in Table H-1. In general, elevated blood pressure is observed 
with greater frequency in older age-groups. Elevated blood pressure was 
more common in black than in white men surveyed in 1976-80 in all age 
groups. However, the slope of increased prevalence with age is different 
for black and white men. 

Large racial differences in rates of elevated blood pressure were 
observed among the 35-44 and 55-64 year-old men (but only at these ages). 
The black-white prevalence differences among the 35-44 year-olds probably 
reflect the younger age of onset of hypertension among blacks compared to 
whites; white rates have "caught up" in the 45-54 year-old group. The 
disparity among the older men (55-64 years of age) may reflect somewhat 
lower proportions of effectively treated hypertensives in black compared to 
white men at these ages (see Table H-3) . The inconsistency in the pattern 
of race difference by age suggests that comparisons based on age-adjusted 
data may be inadequate for some purposes. 



Table H-1. Age-specific and overall prevalence of elevated 

blood pressure in black and white men ages 25-74, 
United States, 1976-1980.* 

rate per 100 population with elevated 
blood pressure"" 

Age-group 25-34 35-44 45-54 55-64 65-74 Total 



Black Men 


11.7 


22.3 


23.0 


39.2 


27.5 


22.4 


White Men 


8.4 


10 .-6 


21.2 


22.3 


24.5 


15.9 


Black minus 














White 


3.3 


11.7 


1.8 


16.9 


3.0 


6.5 



" from Reference 1, Table 5 

•" defined as SBP >=160 mmHg and/or DBP> >=95 mmHg 



As shown in Table H-2, the overall prevalence of elevated blood pressure 
has declined substantially in both black and white men ages 25-74. The 
decline among black men (35.3%) was larger than for white men (11.8%), 
lowering the black-white ratio from 2 . in 1971-75 to 1.45 in 1976-80. The 
highest prevalence of elevated blood pressure among black men was in the 
55-64 year age-group in both surveys. The percent decrease in prevalence 



269 



25-34 




16.4 


35-44 




2>1 .1 


45-54 




34.7 


55-64 




59.9 


65-74 




43.7 


25-74 


Black 


35.7 


15-lk 


Whiter 


18.0 



was relatively consistent across age-groups among black raen--slightly lower 
than the overall 35.3% in the 25-34 year-old men and slightly higher among 
the 35-44 year-old men. 



Table H-2. Percent decline in prevalence of elevated blood 
pressure between 1971-75 and 1976-80, black men 
in age-groups between 25 and 75 and age-adjusted 
for black and white men, U.S. 

rates per 100 population 

1971-75 1976-80 % change* 

11.7 - 28.7 

22.3 - 40.8 

23.0 - 33.7 
39.2 - 34.5 . 
27.5 - 37.1 

23.1 - 35.3 
15.9 - 11.7 

" calculated from rates in reference 4, table II; elevated blood 

pressure defined as SBP >=160 and/or DBF >=95 mmHg. 
# from Reference 4, Table V 



On the surface at least, the data in Table H-2 indicate progress in 
hypertension detection and control between 1971 and 1980 which benefitted 
black men to a relatively greater extent than white men. However, the data 
on hypertension prevalence are only partially helpful in confirming this 
impression of progress in reducing the black-white hypertension disparities 
(Table H-3) . As noted earlier, better coverage of black hypertensives 
theoretically implies improved survival and increased prevalence (assuming 
no decrease in incidence) . The proportion of hypertensives among black men 
ages 25-74 increased between NHES and the NHANES I augmentation survey 
(1974-75) (NHANES la), but then decreased such that prevalence in 1976-80 
was lower than that observed in 1960-62. Although this difference was 
apparently not statistically significant, it is in contrast to what the 
NCHS report identifies as a significant increase in hypertension prevalence 
among white men over the 20 year period (1). The meaning of this trend in 
prevalence is unclear. 

Trends in hypertension awareness, treatment, and control among black 
and white men are also summarized in Table H-3. The interpretation of 
these variables is relatively straightforward and shows considerable 
improvement for men of both races, particularly for black men, in awareness 
and use of medication. The percent of black hypertensive men who had not 
been diagnosed previously dropped sharply between NHES and NHANES la and 
declined further between NHAKES la and NHANES II. Improvements in 



270 



awareness among white men were similar, but of a lesser degree. The 
proportion of unaware hypertensives was nearly 15% greater for black than 
for white men in 1960-62 and nearly 5% less in 1976-80. 

A similar cross -over was observed for the percentage of black 
compared to white hypertensives on medication between NHES and NHANES II: 
a slightly smaller percentage of hypertensive black than white men were on 
medication in 1960-62; a slightly higher percentage of black compared to 
white men were on medication in 1976-80. Levels of awareness were 60% or 
greater among both black and white men; medication use was lower--around 
40%. However, although the extent of control tripled for black men and 
nearly doubled for white men during this period, hypertensive black men on 
medication were less likely than white men to have adequately controlled 
blood pressure in all three survey periods. Overall levels of control were 
still quite low in men (on medication) of both races in 1976-80. 



Table H-3. Rates of hypertension prevalence, awareness, treatment, 
and control, black and white men, ages 25-74, U.S., 
1960-62, 1974-75, and 1976-80-'- 







1960-62 


1974-75 


1976- 


■80 


percent of 


BM 


31.8 


37.1 


28, 


.3 


hypertensives 












in population^ 


WM 


16.3 


21.4 


21, 


.2 


percent of 












hypertensives 


BM 


70.5 


41.0 


35, 


.7 


not previously 












diagnosed 


WM 


56.7 


42.3 


40, 


.6 


percent of 


BM 


18.5 


24.0 


40, 


.9 


hypertensives 












on medication 


WM 


22.4 


25.9 


38, 


,3 


percent of 




-~ 








hypertens ives 


BM 


5.0 


12.7 


16 


.1 


on medication 












whose blood 


WM 


11.8 


15.1 


20 


.9 



pressure was 
control led## 



" Reference 1, Table 7; data are age adjusted to the U.S. population 

at the midpoint of NHANES II (1976-80). 
# defined as either SEP >=160, DBF >=95, or taking antihypertensive 

medication 
## hypertensives on medication and with blood pressures below 

the levels considered as elevated range (below the cut points 

for elevated blood pressure) 



271 



3.1.2.2. Demographic Patterns : Men 

Mean blood pressure levels of black men in 1971-75 were consistently 
higher than those of white men in all four regions of the country. Mean 
blood pressure levels among black men are highest in the Northeast and 
lowest in the West (3, Table 17; age-adjusted rates). Similarly, black men 
had higher mean blood pressure levels than white men in both urban and 
rural areas. The mean blood pressures of black men in rural areas were 
higher than for black men in urban areas (3, Table 18; age-adjusted rates). 
Tabulations by annual family income and level of education indicated higher 
blood pressures among the black compared to white men at each level of 
these variables (3, Tables 19 and 20; age-adjusted rates), with the 
exception that black men with less than 5 years of education had mean blood 
pressures considerably below the rest of the distribution. (Note that 
these are trends in the data and not necessarily statistically significant 
differences . ) 

3.1.2.3 Prevalence of Elevated Blood Pressure and Hypertension 
in Black and White Women, 1960-1980. 

Age-specific and overall prevalence rates of elevated blood pressure in 
black and white women in 1976-80 are shown in Table H-4. Prevalence 
increased with age in women of both races and was 1.7 to 3 times higher in 
black than white women in every age-group. Black-white differentials are 
larger in women over 45 years of age than among younger women (this is also 
the age-group when blood pressure levels of women catch up with and then 
exceed those of men) . 



Table H-4. Age-specific and overall prevalence of elevated 

blood pressure in black and white women ages 25-74, 
United States, 1976-1980.- 

rate per 100 women with elevated 
blood pressure"" 



Age Group 


25-34 


35-44 


45-54 


55-64 


65-74 


Total 


Black Women 


4.3 


17.6 


37.3 


36.4 


43.4 


23.2 


White Women 


2.3 


6.5 


12.1 


18.3 


26.3 


11.4 


Black minus 














White 


2.0 


11.0 


25.2 


18.1 


17.1 


11.8 



" from Reference 1, Table 5 
** defined as SBP >=160 mmHg and/ or DBP >=95 mmHg 



Table H-5 indicates decreases in the prevalence of elevated blood 
pressure among black women in each age-group, but with a considerable 
age-time interaction (i.e., very different levels of decrease in different 



272 



age-groups). The decrease among black women 25-74 years is approximately 
representative of the level of decrease among 35-44 and 55-64 year-old 
women. A very large decrease (65%) was observed among the youngest group 
of women. Minimal decreases were observed in the other two age-groups. 
Unlike black men, who showed proportionately larger overall decreases than 
white men in 1971-1980, the overall decreases in black and white women were 
of the same order. Thus, the ratio of elevated blood pressure prevalence 
in black and white women was constant at 2.2. 



Table H-5 . Percent decline in prevalence of elevated blood 

pressure between 1971-75 and 1976-80, black women 
in age-groups between 25 and 75 and age-adjusted 
for black and white women, U.S. 

rates per 100 population 

1971-75 1976-80 °L change 

4.3 - 65.3'V 

17.6 - 26.3 

37.6 - 4.6 

36.4 - 20.9 

43.4 - 7.1 

24.4 - 20.0 
11.1 - 21.8 

" calculated from rates in Reference 2, Table II; elevated blood 

pressure defined as SBP >=160 and/or DBF >=95 mmHg. 
# from Reference 4, Table 5 



Data on hypertension prevalence (Table H-6) show higher prevalence in 
black compared to white women, with essentially no changes in either group 
over the three survey periods. The 20% decline in the 

prevalence of elevated blood pressure is not accompanied by a change in 
hypertension prevalence (at least not in the overall age-adjusted data) . 
Thus, as discussed earlier, no conclusion is possible regarding changes in 
the survival of women with hypertension over time. Awareness of 
hypertension increased in women of both races and to approximately the same 
degree. More black than white women with hypertension had been previously 
informed of their condition in NHES and NHANES II. In 1976-80 less than 
15% of hypertensive black women and 25% of white women were previously 
unaware of their condition. Approximately 60% of both black and white 
women hypertensives were on medication in the 1976-80 survey. There was no 
racial difference in the proprortion of the women on medication whose blood 
pressures were adequately controlled in either NHES or NHANES II. However, 
the proportion of control approximately doubled over this time period. The 



25-34 




12.4 


35-44 




23.9 


45-54 




39.4 


55-64 




46.0 


65-74 




46.7 


25-74 


Black 


30.5 


25-74 


Whiter 


14.2 



273 



proportion of hypertensive women whose medications were adequately control- 
ling their blood pressure levels was approximately twice that for men. 



Table H-6. Rates of hypertension prevalence, awareness, treatment, 
and control, black and white women, ages 25-74, 
U.S. ,1960-62, 1974-75, and 1976-80--'- 



percent of 
hypertens ives 
in population^/ 

percent of 
hypertens ives 
not previously 
diagnosed 

percent of 
hypertens ives 
on medication 

percent of 
hypertens ives 
on medication 
whose blood 
pressure was 
control led## 





1960-62 


1974-75 


1976-80 


BW 


39.8 


35.5 


39.8 


WW 


20.4 


19.6 


20.0 


BW 


35.1 


28.9 


14.5 


WW 


43.9 


29.7 


25.2 


BW 


48.1 


36.4 


60.6 


WW 


38.2 


48.5 


58.6 


BW 


20.2 


22.3 


38.3 


WM 


21.9 


28.1 


40.3 



" Reference 1, Table 7; data are age adjusted to the U.S. population 

at the midpoint of NHANES II (1976-80). 
# defined as either SBP >=160, DBP >=95, or taking antihypertensive 

medication 
## hypertensives on medication and with blood pressures below 

the levels considered as elevated range below the cut points 

for elevated blood pressure 



3.1.2.4 Demographic Patterns 



Women 



As described for men, blood pressures of black women in 1971-75 were 
higher than those of white women in all four regions, in all types of 
residential areas and at all income and education levels (3, Table 17-20; 
age-adjusted rates). Regional patterns of blood pressure are different in 
black men and women. Whereas blood pressures among black men in the 
Northeast were highest, the highest levels among black women were in the 
South and West. Rural black women had higher blood pressures than those in 
urban areas. In tabulation by educational levels, black women with less 
than 5 years of education were noticeably different from the rest of the 
blood pressure distribution, but blood pressure levels were higher in this 
group of women- -not lower, as observed in men (note that these are trends 
from tables and not necessarily significant) . 



274 



3.2 Left Ventricular Hypertrophy (LVH) 

Left ventricular hypertrophy (LVH) , a putative independent risk factor 
for IHD, is a lethal marker (7,8). LVH in the general adult population is 
primarily due to prolonged blood pressure elevations (7). It was an 
antecedent finding in 45% of all cardiovascular deaths in the Framinghara 
Study (9). The five-year mortality rate in Framingham men who developed 
ECG-LVH was 35% compared to approximately 10 to 15% or less expected 
otherwise (9). For women, 20% of those who developed ECG-LVH were dead 
within five years. For those aged 65 years and older these mortality rates 
were 50% and 35%, respectively. Kannel has suggested that the excess 
mortality associated with ECG-LVH may not be attributable to associated 
hypertension since ECG-LVH carried three times the risk of hypertension 
without the ECG finding (9). On the other hand, the degree of hypertension 
may not have been comparable in those with and without ECG-LVH since the 
clinic blood pressures used to define hypertension in the Framingham study 
may not have adequately reflected degree of hypertension (e.g. by not 
adequately reflecting variations in 24-hour blood pressure or duration of 
hypertension). The mortality rate associated with possible LVH was 
one-half that of definite ECG-LVH. Chest x-ray LVH was associated with 
one-third the cardiovascular mortality rate of ECG-LVH (9). 

Risk of cardiovascular morbidity is also markedly increased in those 
with ECG-LVH. In age 40 year-old Framingham men with systolic blood pressures 
of 195 and positive status on glucose intolerance and cigarette smoking, 
ECG-LVH raises the eight-year probability of cardiovascular disease from 459 
per 1000 to 708 per 1000 (10). ECG-LVH confers a 2 to 9-fold increased risk 
of stroke, cardiac failure, coronary disease and peripheral arterial 
disease (9) . 

In the HDFP, age-adjusted five-year total mortality in the stratum with 
mild hypertension at baseline (stratum I) was approximately double in white 
and black Referred Care males who were LVH positive compared to LVH 
negative by ECG (11). 

The prevalence of ECG-LVH is greater in blacks than whites for both 
sexes (8) . These prevalence differences are clearly demonstrated in 
baseline data for 10,940 HDFP participants, as shown below (Table P-1). 
These baseline prevalence patterns were evident after adjustment for age 
and blood pressure level (12). The prevalence of ECG-LVH was progressively 
higher in HDFP Strata II and III (baseline diastolic blood pressure 105-114 
and 115+ mmHg) vs. stratum I (baseline DBF 90-104 mm Hg) (13). Percentages 
in stratum III were more than 3 times those in stratum I, suggesting a dose 
response relationship. Race-sex specific baseline ECG-LVH prevalence data 
by blood pressure strata have also been published (13,14). 



275 







n 


White 


men 


1892 


Black 


men 


1064 


White 


women 


1185 


Black 


women 


1344 



Table P-1. Baseline prevalence of ECG-LVH by race-sex and 
randomization group for HDFP participants (ages 
(30-69 years, n=10,940) * 

Percent of Subgroup 
Stepped Care n Referred Care 

2.4 1861 3.1 

8.5 1084 9.0 

1.8 1156 1.7 

7.9 1354 7.8 

from Reference 13, Table 2 . 3--". . .based on combined R-wave and 
ST-T segment changes: tall R-wave (Minnesota Code 3.1) and 
major ST segment depression (Minnesota code 4.1-4.3) or major 
T-wave inversion (Minnesota code 5.1-5.3)" 



The reasons for the black excess of ECG-LVH are unclear. Since the 
differences are observed within each stratum of baseline blood pressure 
among the HDFP participants, these racial differences for given levels of 
blood pressure may be indicative of the inadequacy of our usual measures of 
blood pressure (e.g., one to three blood pressures in a clinic 
setting) (7 ,8) . Earlier onset and longer duration of blood pressure in 
blacks are likely contributors (8). Duration of blood pressure elevations 
is difficult to ascertain. Assessment of a possible association with 
ECG-LVH is further complicated by duration and type of antihypertensive 
treatment (7,15-17). Regression of ECG-LVH with antihypertensive treatment 
was observed in the HDFP (18). An additional or alternative explanation 
for black-white differences in LVH prevalence is that the left ventricular 
response to a given blood pressure elevation is greater in blacks than in 
whites (8,19,20). 

Echocardiography (echo) detects LVH earlier than either ECG or chest 
x-ray (15,21). Echo has the greatest sensitivity and specificity of the 
three diagnostic tools (7,15,21). Thus, the prevalence of echo-LVH is 
higher than LVH by ECG in a given population (7) . The proportion of 
echo-LVH cases which progress to ECG-LVH and the proportion of the latter 
which survive to be ascertained have not been documented. The prognostic 
significance of LVH by echo rather than ECG criteria has been uncertain. 
However, recent data from Framingham have documented a significant 
association of echo-LVH with all-cause mortality, independent of standard 
risk factors (22). In that study, approximately twice as many of the men 
and women about age 70 at time of echo measurement) who died (compared to 
those alive) in a two-year period after examination had echo LVH. However, 
only 7% of the women who died and none of the men had LVH by ECG. 

Data on the prevalence of echo-LVH are limited. Reference data for 
whites have been reported from Framingham (7) . There are no 
population-based echo-LVH reference data for blacks. Small-scale studies 
in American and African blacks have documented the presence of 



276 



significantly higher LV wall thickness, interventricular septal thickness, 
LV mass or mass index and lower LV fractional shortening in hypertensives 
vs. normotensive controls (23,25), and proportionate to the level of blood 
pressure. These patterns are reportedly simil?->- to those observed in 
whites and in Japanese (8) . 

Dunn et al. (20) observed higher LV mass index (LV mass per square 
meter of body surface area) in 30 black hypertensives compared to 
age-sex-blood pressure matched controls. Posterior wall thickness was 
correlated to blood pressure and total peripheral resistance in the black 
but not white subjects in that study. Hammond et al . (19) similarly found 
greater echo target organ changes in blacks matched for blood pressure 
levels with whites. 

Savage et al. (23) found that echo findings were similar between black 
and white hypertensive subjects carefully matched for several possible 
conf ounders : age, sex, treatment status, level and known duration of 
hypertension, and renin subgroup. If the origin of black-white echo-LVH 
differences is related to blood pressure variables, then the matching 
protocol and inadequate power (n=35 blacks and 35 whites) in this study may 
have obscured these differences. 

Hammond et al. (19) have reported results of echo-LVH comparisons in 
an occupationally-based sample of black and white normotensive (n=75) and 
hypertensive (n=132) men and women in New York City. The hypertensives in 
this study included newly identified hypertensives defined as (DBP>=95 
mmHg, SEP >=160 mmHg or both, sustained on three occasions over a three 
week period and not previously taking antihypertensive medications. 
Hypertensives also included persons receiving antihypertensive medications 
before joining the study, regardless of blood pressure level at screening. 
No echo variables were different between black and white normotensives , 
suggesting that the echo baseline in blacks and whites was the same. Among 
the hypertensives, LV mass index was similar in blacks and whites but 
relative wall thickness, cardiac output and total peripheral resistance 
were higher in blacks. Blood pressures of the black and white 
hypertensives were similar. Differences observed may be explained in 
various ways including either different durations (and/or actually 
different severity of hypertension) or differential effects of blood 
pressure elevations. 

In the New York City study (19), progression of LVH in the newly 
diagnosed, untreated hypertensives was not differentiated from possible 
regression of left ventricular measurements towards normal in the 
hypertensive subjects on medications at the time of screening. Differences 
in echo findings in the two groups were not observed at the time of study 
but may have been present at one time. Three studies (16,17,26) documenting 
regression of echo-LVH in hypertensives with antihypertensive treatment 
have included blacks. One of these studies (16) reported regression very 
early in therapy (at one month) which was sustained during treatment over 
an 18 month follow-up period. It is noteworthy, however, that methyldopa 
but not hydrochlorothiazide, was associated with regression of echo-LVH. 
Diuretics (e.g. hydrochlorothiazide) are often recommended as the preferred 



277 



treatment for blacks (27). Much more information is needed regarding the 
significance of regression of echo-LVH (and other changes) in response to 
various antihypertensives. If differing hypertensive regimens are 
recommended for black and white hypertensives on a racial basis (27) the 
potential significance of such information is obvious. 

More information is also needed about how representative clinic blood 
pressures are. This is suggested by the 10 year prospective study of 
Perloff et al. (28), showing prognostic significance of ambulatory blood 
pressure independent of clinic blood pressures. 

In summary, if blood pressure elevation of long duration is 
related to LVH (which is true (7)) and if LVH then becomes established as 
an independent IHD risk factor (which appears to be true (22)), then the 
attributable risks of LVH in blacks may be greater than in whites. As 
noted above, the onset of blood pressure elevations in blacks occurs at an 
earlier age than in whites. The prevalence of such elevations is also 
greater in blacks. Finally, early (echo) LVH and late (ECG) LVH may be 
greater in blacks than in whites with the same apparent level of blood 
pressure elevation. 



ACKNOWLEDGEMENTS 

We gratefully acknowledge the editorial assistance of Sandra 
J. Anderson and Elisabeth Pitt. 



278 



3.3 References 

1. Rowland M, Roberts J. Blood pressure levels and hypertension 
in persons ages 6-74 years. United States 1976-80. NCHS . 
Vital and Health Statistics. AdvanceData No. 84, October, 1982. 

2. National Center for Health Statistics. Blood pressure levels 

of persons 6-74 years, 1971-1974, Roberts J., Maurer K. Vital and 
Health Statistics. Series 11. No. 203. DHEW Pub. (HRA) 78-1648. 
September, 1977. 

3. National Center for Health Statistics. Hypertension in adults 25-74 
years of age. United States 1971-75, Roberts J, Rowland, M. Vital and 
Health Statistics. Series 11. No. 221. PHHS Pub. No. (PHS) 81-1671. 
April, 1981. 

4. Rowland ML, Fulwood R. Coronary heart disease risk factor trends in 
blacks between the first and second National Health and Nutrition 
Examination Surveys, United States 1971-1980. Am Heart J 1984; 108: 
771-779. 

5. Oni A. Intraracial factors in blood pressure variations among the black 
population. J Natl Med Assoc 1984; 76:594-603. 

6. Hypertension Detection and Follow-up Program Cooperative Group. Five-year 
findings of the Hypertension Detection and Follow-up Program. 

II. Mortality by race, sex, and age. JAMA 1979;242:2572-2577. 

7. Savage DD, Abbott RD, Padgett S, Anderson SJ, Garrison RJ. 
Epidemiologic features of left ventricular hypertrophy in 
normotensive and hypertensive subjects. In Cardiac Left 
Ventricular Hypertrophy, HEDJ ter Keurs , JJ Schipperheyn, 

eds. Martinus Nijhoff. 1983, pp. 3-15. . 

8. Savage DD. Echocardiographic assessment of cardiac anatomy 
and function in black and white hypertensive subjects. 

In Textbook of Ethnic Medicine, R Williams ed (in press). 

9. Kannel WB . Left ventricular hypertrophy in hypertension: 
prognostic and pathogenetic implications. The Framingham 
Study. In The Heart in Hypertension, Strauer BE ed. 1981, 
p. 123. 

10. Kannel WB. An overview of the risk factors for cardiovascular 
disease. In Prevention of Coronary Heart Disease. Practical 
Management of the Risk Factors, Kaplan NM, Stamler J, eds. 
Philadelphia: W.B. Saunders Company. 1983, Chapter 1, pp. 1-19. 

11. Tyroler HA. Overview of risk factors for coronary heart 
disease in black populations. Am Heart J 1984;108:658-660. 



279 



12. The HDFP Cooperative Group, presented by Prineas R. Sex 
and race differences in end organ damage among 10,940 
hypertensives. Am J Cardiol 1978:41 : 402 (abstract) . 

13. Taylor JO, Borhani NO, Entwisle G, Farber M, Hawkins CM, 
on behalf of the HDFP Cooperative Group. Summary of the 
baseline characteristics of the hypertensive participants. 
Hypertension 1983 ;5 (part II, no.6):IV-44 - IV-50. 

14. Hypertension Detection and Follow-up Program Cooperative 
Group. Five-year findings of the Hypertension Detection 
and Follow-up Program. Mortality by race-sex and blood 
pressure level. A further analysis. J Comm Health 1984; 9: 
314-327. 

15. Savage DD, Devereux RB. Echocardiography and hypertension. 
Primary Cardiology. 1981;7:137-149. 

16. Wollam GL, Hall WD, Porter VD, Douglas MB, Unger DJ, Blumstein 
BA, Costonis GA, Knudtson ML, Felner JM, Schlant RC . Time 
course of regression of left ventricular hypertrophy in 
treated hypertensive patients. Am J Med 1984;75:100-110. 

17. Schlant RC, Felner JM, Blumstein BA, Wollan GL, Hall WD, 
Shulman NB, Heynsfield SB, Gilbert CA, Tuttle EB . Echo- 
cardiographic documentation of regression of left ventricular 
hypertrophy in patients treated for essential hypertension. 
Eur Heart J 1982;3(supp A): 171-175. 

18. The Hypertension Detection and Follow-up Program Cooperative 
Group. Regression of left ventricular hypertrophy (LVH) 
with anti-hypertensive therapy. Circ 1981;64(Supp IV); 
IV-322 (abstract). 

19. Hammond IW, Alderman MH, Devereux RB, Lutas EM, Laragh 

JH. Contrast in cardiac anatomy and function between black 
and white patients with hypertension J Natl Med Assoc 
1984;76:247-255. 

20. Dunn FC, Chandraratna P, de Carvalho JGR, Basta LL, Frohlich 
ED. Pathophysiologic assessment of hypertensive heart 
disease with echocardiography. Am J Cardiol 1977;39:789-795. 

21. Savage DD, Drayer JIM, Henry WL, Matthews EC Jr, Ware JH, 
Gardin JM, Cohen ER, Epstein SE, Laragh JH. Echccardiographic 
assessment of cardiac anatomy and function in hypertensive 
subjects. Circulation, 1979;59:623-32. 



280 



22. Savage DD, Garrison RJ, Castelli WP, Kannel WB, Anderson 

SJ, Feinleib M. Echocardiographic data from Framingham and newer 
studies of echocardiography. Echocardiographic left ventricular 
hypertrophy in the general population is associated with increased 
2-year mortality, independent of standard coronary risk 
factors. AHA Council on Epidemiology (invited paper), 1985. 

23. Savage DD, Henry Wl, Mitchell JR, Taylor AA, Gardin JM, 
Drayer JIM, Laragh JH. Echocardiographic comparison of 
black and white hypertensive subjects. J Natl Med Assoc 
1979;71:709-712. 

24. Schlant RC, Felner JM, Heynsfield SB, Gilbert CA, Tuttle 
EB, Blumenstein BA. Echocardiographic studies of left 
ventricular anatomy and function in essential hypertension. 
Cardiovas Med 1977;2:477-491. 

25. Adesanya CO, Sanderson JE, Verheihen Ir PJY, Brinkman AW: 
Echocardiographic assessment and systolic time interval 
measurements in the evaluation of severe hypertension in 
Nigerian Africans. Aust NZ J Med 1981;11:364-369. 

26. Devereux RB , Savage DD, Sachs I, Laragh JH. Long-term 
effects of hypertension on the heart. Clin Res 1980; 28: 
330A (abstract). 

27. The 1984 report of the Joint National Committee on Detection, 
Evaluation, and Treatment of High Blood Pressure. The Joint 
National Committee on Detection, Evaluation, and Treatment 

of High Blood Pressure. Arch Intern Med 1984;144:1045-1057. 

28. Perloff D, Sokolow M, Cowan R. The prognostic value of 
ambulatory blood pressures. JAMA 1983;249:2792-2798. 



SUPPLEMENTAL REFERENCES 

S-1. Folkow B, Nordlander MIL, Strauer B-E, Wikstrand J eds . 

Pathophysiology and clinical implications of early structural 
changes. Hypertension 1984;6 : (Suppl 3)iii-l - iii-187. 

S-2. Messerli RH, Schlant RC , eds. Proceedings of a Symposium: 
Left Ventricular Hypertrophy in Essential Hypertension. 
Am J Med 1983;75:1-120. 

S-3. Panidis IP, Kotler MN, Ren J-F, Mintz GS , Ross J, Kalman P. 
Development and regression of left ventricular hyertrophy. 
J Am Coll Cardiol 1983;3:1309-1320. 

S-4. Tarazi RC. Regression of left ventricular hypertrophy: partial 
answers for persistant questions (editorial). J Am Coll Cardiol 
1983;3:1349-1351. 



281 



4.0 CONCLUSION 

Our review suggests that intensified efforts to understand and reduce 
black-white differentials in hypertension (and, possibly, left ventricular 
hypertrophy) and obesity (black women) offer the greatest opportunity among 
the standard and putative independent cardiovascular risk factors for 
reduction of cardiovascular morbidity-mortality disparities between blacks 
and whites. These intensified efforts should of course be in the context 
of continued vigorous efforts to reduce all of the cardiovascular risk 
factors in both blacks and whites. 



282 



Relationship of Social Class 
to Coronary Disease Risk 
Factors in Blacks: 
Implications of Social 
Mobility for Risk Factor 
Change __^____„ 




Lucile L. Adams, Ph.D. 

Department of Epidemiology 
Graduate School of Public Health 
University of Pittsburgh 
Pittsburgh, Pennsylvania 



Laurence O. Watkins, M.D., M.P.H. 

Section of Cardiology 
Medical College of Georgia 
Augusta, Georgia 

Lewis H. Kuller, M.D., Dr.P.H. 

Chairman, Department of Epidemiology 
Graduate School of Public Health 
University of Pittsburgh 
Pittsburgh, Pennsylvania 

DanielD. Savage, M.D., Ph.D. 

Medical Advisor 

National Center for Health Statistics 

Hyattsville, Maryland 

Richard Donahue, Ph.D. 

National Heart, Lung, and Blood Institute 
Bethesda, Maryland 

Ronald E. LaPorte, Ph.D. 

Department of Epidemiology 
Graduate School of Public Health 
University of Pittsburgh 
Pittsburgh, Pennsylvania 



Coronary heart disease (CHD) is the leading cause of death among United 
States blacks, mortality rates being similar in black and white men and 
greater in black women than in white women (1). National survey data from 
1962 revealed similar CHD prevalence rates for blacks and whites (2). Small 
studies in two southern states have revealed lower CHD incidence in black than 
in white men in the period 1960-1974, and greater CHD incidence in black than 
in white women (3,4). Among both men and women, black rates of admission to 
the hospital with the diagnosis of acute myocardial infarction are lower than 
those of whites (5). These data on the CHD experience of blacks are 
conflicting, but it is clear that compared to whites, blacks have a greater 
prevalence of CHD risk factors including hypertension, cigarette smoking, and 
among middle-aged women, obesity and diabetes mellitus (6). It is somewhat 
paradoxical that black men in particular do not have higher CHD rates than 
whites. 

This paradox would be intensified if, as has been hypothesized, there is 
an inverse relationship between social class and risk of CHD. A 1968 review 
of this subject by Antonovsky (7), and a more recent one by Jenkins (8), have 
discussed the conflicting data with regard to CHD in white populations. Some 
studies suggest higher risk of CHD with high social status, while others 
indicate a lower risk. An explanation for these diametrically opposed results 
has been proposed by Morgenstern (9). Guided by Cassel, he suggested that the 
association of CHD risk with social status might have been altered during the 
period of rapid social change in urban populations in the U.S. in the period 
1930-1950. In this formulation, among individuals and groups which came to 
enjoy the benefits of rapid industrial growth, those of high socioeconomic 
status (SES) initially asssuraed high CHD risk status, but as they adapted more 
rapidly to the new material conditions by altering lifestyles, they became at 
significantly lower risk than their low SES counterparts. 

Such links as exist between SES and CHD risk may be mediated by causal 
links between SES and lifestyle, and between lifestyle or lifestyle changes 
and biological risk factors. In this hypothetical framework, low or high SES 
may be linked to CHD risk because of an association with adverse risk factor 
distributions, or SES may modify the effect of the major biological risk 
factors on CHD incidence. In an investigation of the data on CHD prevalence 
(1960), incidence (1960-1967), and mortality (1960-1974) in the white adult 
population of Evans County, Seorgia, Morgenstern found evidence of a change in 
the predicted direction for the association between SES and CHD in men (9) 
That is, the prevalence of CHD was initially higher in white men of high SES, 
but during follow-up, the incidence of CHD was lower in the cohort of 35-54 
year old men of high SES. In addition, there was evidence that the changing 
relation between SES and CHD risk was partly due to differential change in 
certain biological risk factors, especially hypertension. That is, there was 
greater adverse risk factor change among younger low SES men. In addition, 
there was no evidence that SES modified the effect of the major biological 
risk factors on CHD. 

Because of systematic discrimination, the black population of the U.S. 
has been largely of low SES (10). In the last 20 years, there have been rapid 



285 



socioeconomic changes in certain segments of the black population (11), and 
some black families have experienced upward mobility, either within a 
generation or between successive generations. In view of such changes, the 
implications of Morgenstern' s hypothesis and observations for the associations 
betwen SES and CHD incidence and between SES and CHD risk factor distributions 
in blacks are important, but no systematic examination of this subject has 
been done (12-14). 

This review will summarize the data on 1) the extent and characteristics 
of socioeconomic change in blacks since 1960; 2) The relation between SES and 
CHD incidence and mortality in blacks; 3) the cross-sectional associations 
between SES and related factors and the prevalence (and incidence) of CHD risk 
factors; and 4) the risk factor characteristics of black population samples 
from the higher end of the socioeconomic spectrum. The latter will be 
discussed as examples of black populations which may have experienced upward 
mobility, either recent or remote, and which might make manifest the impact of 
such mobility on CHD risk factors. 

Socioeconomic Status Changes in Blacks 

In the period 1960-1981, there were increases in the percentage of black 
adults above age 25 years who completed high school or four years of college 
(15). By 1981, the median number of years of schooling for black males and 
females exceeded 12, and the black-white difference was less than one year. 
During these two decades, the median duration of formal education had 
increased by 4.4 years for black males, and 3.5 years for black females, but 
by only 1.9 and 1.3 years for white males and females, respectively. These 
changes in educational attainment were associated with changes in the 
occupational profile of blacks. There has been an increase in the percentage 
of blacks who are white-collar workers, and a decline in the percentage of 
farm workers. Between 1972 and 1981, the percentage of blacks employed in 
professional, technical, managerial or administrative jobs increased from 
11.2% to 15.7% (16). However, despite the broader range of occupations now 
held by blacks, especially black women, the majority of blacks, especially 
men, remain blue-collar or service workers. Blacks remain more likely to be 
unemployed (17). The black unemployment rate in 1982 was 17.3%, compared to 
8.6% for whites. This 2:1 ratio has remained virtually unchanged since 1960. 
Blacks who are unemployed are likely to remain so for longer periods of time. 

Family incomes remain substantially lower among blacks than whites (15). 
This is so, particularly for families headed by women. It is noteworthy that 
the financial rewards of education are dissimilar for blacks and whites. Only 
18.1% of white families in which the head of the household has at least four 
years of college earn less than $20,000 per year. The comparable number for 
black families is 34.7%. Similarly, 35.5% of white families whose heads of 
household have four years or more of college earn more than $40,000 per year, 
while only 18.1% of similar black families have such incomes. The disparity 
is more striking, if it is noted that of all black families in which the 
householder has at least four years of college, 23.7% earn less than $15,000 
per year, a proportion similar to that for white families in which the 



286 



householder has four years of high school (26.1%). Income disparities between 
blacks and whites appear to be attributable to differences in pay-rates for 
black and white men holding the same types of jobs (18), and more to 
restriction in the job opportunities open to blacks once they have completed 
their education, than to differences in educational attainment. 

These considerations serve to emphasize that a relatively small 
proportion of a black population can be considered "upwardly mobile". Social 
mobility refers to the movement of an individual from one social position to 
another different from the one to which he/she was accustomed. For the 
individual, there are different types of social mobility and the 
classification depends on the reference point (14). Intergenerational 
mobility takes into account the social position of offspring with respect to 
that of the parents. This can be compared to intragenerational or career 
mobility which takes account of changes experienced by the same individual 
within his/her lifetime. As a consequence of recent social change, some 
blacks have experienced intergenerational mobility, and others 
intragenerational mobility, or even both. In the course of this report we 
shall examine data on groups of blacks in whom upward mobility is presumed to 
have occurred in current or recent generations, by virtue of their superior 
educational attainment and social position compared to the general black 
population. 

One of the samples of blacks which shall be considered "upwardly mobile" 
for the purpose of this review is constituted of college students. This 
appears reasonable, since data from a national study of male college students 
which examined occupational expectations according to race and socioeconomic 
background reveal that among blacks, the level of education of the father is 
an important determinant of career aspirations, college performance and 
occupational expectations (19). Professional orientations of black college 
students may reflect the orientations and experiences of high-achievement 
parents . 

Socioeconomic Status, Social Mobility and CHD Incidence. - 

As a prelude to consideration of the limited data on blacks, observations 
on white U.S. populations will be reviewed. The observations in Evans County, 
Georgia have been noted briefly (3). In the 1960 prevalence study, high-SES 
white men had a CHD prevalence rate 2 or 3 times that of lower SES white men. 
The 1960-1967 incidence study showed that high SES was associated with higher 
CHD incidence for white men over age 55 years, but was inversely related to 
CHD incidence in white men 35-54- years of age. In this study, SES was 
assessed by use of the McGuire-White index which takes account of occupation, 
education, and source of income of the head of each household. 

Studies in white populations which have used education as the marker of 
SES have suggested that education is associated with lower CHD incidence. For 
example, Hinkle et al (20) observed that the incidence of new CHD events and 
deaths was approximately 30% lower among college-educated men than among non- 
college-educated men. On the other hand, the association between CHD 



287 



incidence and occupation may be different from that observed for education. 
In a 1957 study of CHD incidence in North Dakota, Syrae et al (21) found that 
the incidence of CHD was higher among white-collar workers than among blue- 
collar or agricultural workers. An analysis which took account of the 
occupation (agricultural or non-agricultural) of each subject's father, 
indicated that the excess risk was confined to those white-collar workers from 
an agricultural (i.e., rural) background (22). 

Studies of career or intragenerational occupational mobility among whites 
have also detected higher rates of coronary disease among the mobile than 
among the nonmobile. Syme et al (22) made such observations on coronary 
incidence in North Dakota, and similar cross-sectional observations on CHD 
prevalence in an urban area in California (23). In the North Dakota Study 
(22), Syme et al noted significantly higher CHD incidence rates in the group 
of men who had made four or more major job changes since age 18 years 
(compared to those with one or no job changes), and the group of men who had 
made two or more major cross-country moves since age 18 years (compared to 
those who had made one or no such moves). The CHD incidence rates were 
significantly higher in the "highly mobile" group (the entire group of white- 
collar workers with paternal agricultural background, and all men with high 
occupational or geographic mobility) than in the stable group (farmers with 
paternal agricultural background) or the remaining "moderately mobile" group. 
The analyses suggested that the contribution of sociocultural mobility t^ CHD 
incidence was independent of cigarette smoking, blood presssure, and body- 
weight. The necessity for such analyses is illustrated by a report from the 
Tecumseh Community Health Study (24). In men and women, ages 35-69 years, 
residential mobility and urban residence, particularly in childhood, were 
related not only to the prevalence of CHD, but also to hypertension and 
cigarette smoking. 

Kaplan et al (25), in the initial Evans County report, noted that the 
prevalence of CHD in white men was higher in upwardly mobile men from the 
lower social classes than among those who were not mobile. The observation 
discordant with those of Syme et al (22) was that upward mobility among the 
upper social classes was associated with CHD prevalence rates lower than those 
among the nonmobile. Other data on the relationship of sociocultural mobility 
and CHD incidence have been obtained from a follow-up study of 13,728 male 
Harvard University students. Gillum and Paffenbarger (26) observed that 
individuals who exhibited intergenerational mobility (that is, their social 
class was eventually higher than that of their fathers) had a 1.5 times higher 
risk of fatal CHD and MI than those who did not experience such mobility. 

A single study has examined the relationship between SES and CHD 
incidence in blacks in and around Charleston, South Carolina, and one recent 
analysis may cast some light on the relationship between SES and CHD mortality 
in urban blacks in Los Angeles, California. In the Charleston Heart Study 
(4), a special cohort of high-SES black men was assembled by peer nomination. 
Over 14 years of follow-up (1960-1974), the incidence of CHD in this group of 
men was less than half of that in the predominantly low-SES men in the random 
population sample. In this study, SES was assessed on the basis of occupation 



288 



and income. The risk characteristics of the high-SES group have not been 
specifically reported, though one publication from the Charleston Heart Study 
has revealed that the incidence of hypertension was 3-4 times as high in low- 
SES as in high-SES men (27). This particular observation is similar to the 
Evans County finding in white men. 

Frerichs and coworkers examined the association betwen income and 
cardiovascular disease mortality rates in 1979-1981 in Los Angeles County 
(28). In this study, they determined the median family income in each census 
tract, assigned this value to the resident population and to individual 
residents who died, and aggregated census tracts into five income groups. The 
age-adjusted mortality rate from Diseases of the Heart (International 
Classification of Disease Codes 390-398, 402, 404-429) was inversely related 
to income. The contribution of ischemic heart disease (ICD 410-414) to the 
age and sex-adjusted mortality rate for diseases of the heart was 62.6% for 
the entire county, 53.7% for blacks, and 63.4% for whites. The age-adjusted 
ischemic heart disease mortality rate of black men was 18% lower than that 
recorded for white men, 223.9 compared to 274/100,000, while the rates for 
women were virtually identical, 158.1 and 158.5/100,000. The inverse 
association between mortality from diseases of the heart and income was common 
to both blacks and non-blacks. Compared to black men in the higher income 
group (_> $28,500), black men in the lowest income group (_< $13,600) had a 53% 
excess risk of death from diseases of the heart. The risk differential for 
women was 33%. Such analyses were not performed for deaths from ischemic 
heart disease, but since they constitute the majority of the deaths in 
question, a similar relationship to income is likely. No study of 
intragenerational or intergenerational mobility (social, cultural, 
occupational or geographic) and CHD incidence in blacks has been reported 
(14). 

SES and CHD Risk Factor Associations in Blacks 
Hypertension 

Among both blacks and whites, there is a distinct inverse association 
between SES and blood pressure. For example, Syme et al (29) assessing SES in 
1968-1969 on the basis of education and occupation, detected a higher 
prevalence of hypertension in blacks of low SES. Similarly, as noted earlier, 
in Charleston County, South Carolina, the incidence of hypertension in 1960- 
1974 in black men was inversely related to social class (27). In a black 
Baltimore population (30), there was also an inverse association between 
income and the incidence of hypertension in 1973-1977. Over this 3-4 year 
period, the incidence of hypertension in sons of professionals was 
approximately one quarter of that observed in sons of laborers. 

The relationship between the prevalence of hypertension and the duration 
of formal education was also striking in the screening conducted in 1973-1974 
for the Hypertension Detection and Follow-Up Program (31). I-" blacks with 
less than 10 years of education, the prevalence of hypertension was 43.9%, 
while in those who had completed college, the prevalence was 27.7%. For 
whites, the corresponding rates were 23.1% and 13.5%. Mean systolic and 



289 



diastolic blood pressures in adults ages 18 to 74 years examined by NHANES II 
(1976-1980) were inversely related to the duration of formal education of 
examinees in all race and sex groups, the association being more marked for 
women than for men (32). The prevalence of definite hypertension (systolic 
blood pressure 160 mmHg or greater or diastolic blood pressure 95 mmHg or 
greater, or taking antihypertensive medication) showed a slight, not 
statistically significant, decline between 1960 and 1980 in black adults (32), 
coincident with their increased educational attainment. 

In Bogalusa, Louisiana, among black children ages 5-14 years examined in 
1973-1974, those whose parents had a postgraduate education had lower systolic 
blood pressures than did similar white children. In addition, there were no 
racial differences in systolic and diastolic blood pressure between children 
of white-collar workers (33). These findings are in contrast to the 
significantly higher blood pressure levels observed among black children after 
statistical control for education and occupation, when the entire group of 
children in the community sample was used as the basis for racial comparisons. 

Elevated Serum Cholesterol 

In NHANES I (1971-1975), serum cholesterol levels were significantly 
higher in the lowest socioeconomic class (on the basis of education and 
income) among whites, but not among blacks (34). There was no clear 
relationship of cholesterol level to education among black men ages 18-74 
years, but among women, serum cholesterol level was generally lower among 
those of higher income. Across income levels, black women had generally lower 
mean serum cholesterol levels than did white women. 

Examination of the impact of parental social status on risk factor 
variables in 5-14 year old children in Bogalusa, Louisiana in 1973-1974 
revealed that black children had significantly higher total serum cholesterol 
levels and alpha lipoprotein (HDL-choles terol) after account was taken of 
parental education and occupation (33). However, among children whose parents 
had a postgraduate education, blacks tended to have lower total serum 
cholesterol and HDL-cholesterol as well as higher pre-beta lipoprotein 
cholesterol (VLDL) than white children. Among children of white-collar 
workers, there were no statistically significant differences between the 
groups for total cholesterol and HDL-cholesterol. 

High Density Lipoprotein Cholesterol 

There is limited information concerning the relationship of SES to HDL- 
cholesterol in blacks. Most of the studies which have evaluated HDL- 
cholesterol levels in blacks have examined low-SES poulations. Among U.S. 
adults, black males have higher HDL-cholesterol levels than white males, while 
the levels for black females are comparable to those of white females (35). 
In the Lipid Research Clinics Program (1971-1976), a direct association was 
detected between SES (measured by education) and HDL-cholesterol in white 
subjects. The black sample in this study was too small to permit such an 
evaluation. 



290 



The Framingham Minority Study evaluated a sample of well-educated blacks 
in Framingham, Massachusetts in 1980 (36). It is remarkable that the age- 
adjusted HDL-cholesterol levels observed in this population are lower than 
those of whites, and lower than those reported for other U.S. black 
populations (37). The educational attainment of this black population was 
such that 56% had completed four years of college. Wilson et al (36) 
speculated that blacks of middle-and upper-SES (a correlate of relatively high 
educational attainment) might have lipoprotein profiles different from those 
reported in lower-SES groups. Data on men recruited into the Multiple Risk 
Factor Intervention Trial (1973-1976) are in accord with this hypothesis (38). 
In this study, mean HDL-cholesterol levels of black men were significantly 
higher than those of white men, but in a multiple regression analysis which 
took account of age, cigarettes smoked per day, diastolic blood pressure, 
number of alcoholic drinks consumed per week, and body mass index, 
socioeconomic status was inversely related to HDL-cholesterol concentrations 
in black men, but directly related to HDL-cholesterol concentrations in white 
men. The black-white differences in HDL-cholesterol levels were largest among 
those of lower SES and were smaller at higher SES levels. 

Cigarette Smoking 

There are relatively few data available on the association between SES 
and cigarette smoking in blacks. Data from the 1970 Health Interview Survey 
indicate that within industries, substantially higher percentages of 
individuals in the lower occupational ranks (where blacks are overrepresented) 
smoke (39). In the Princeton School District Study (40), there was an inverse 
relationship between SES (assessed by education and occupation of the head of 
the household) and the prevalence of cigarette smoking among both black 
children and adults. 

Comparison of data from two successive National Health and Nutrition 
Examination Surveys (NHANES I and II, 1971-1975 and 1976-1980) (41), indicates 
that the prevalence of smoking declined in black men and women between the 
surveys, more among women than among men. The proportion of black adults who 
were heavy smokers (25 or more cigarettes per day) did not change 
significantly, indicating that the decrease in the prevalence of smoking was 
due to a reduction in the ranks of light or moderate smokers. Data derived 
from interviews performed between 1970 and 1980 of hospitalized black adult 
patients yield some information on the prevalence of cigarette smoking in two 
educational strata, high school or less, and college or more (42). They 
indicate that the prevalence of cigarette smoking was lower among college- 
educated black men than among black men with less education, and there was a 
more marked increase in the proportion of former cigarette smokers among the 
college-educated men in the second five-year period. Among black women, the 
prevalence of cigarette smoking was similar in the two educational strata in 
both periods, 1970-1975 and 1976-1980, though the prevalence had declined in 
both groups by about 15% during the period between 1976-1980. These data 
suggest that smoking cessation is more likely among those with more education. 
This is consistent with data from the 1970 Health Interview Survey which 
revealed that smokers in the higher occupational ranks are more likely to 



291 



cease smoking (39). Also, other survey data (43), indicate that black smokers 
who earn more than $15,000 per year, and those who report regular medical care 
are more interested in quitting smoking and report enjoying smoking less than 
do those with lower income and less access to health care. 

Obesity 

The relation of SES and obesity in blacks is largely unexplored. 

Physical Activity 

There is a paucity of literature that evaluates physical activity levels 
in blacks. The limited information from one available study suggests no 
difference in physical activity levels between blacks and whites. In the 1977 
National Health Interview Survey (44), respondents were asked to rate their 
own level of physical activity relative to other persons of their age: more 
active, about as active, or less active. Self-perceived levels of physical 
activity were similar in blacks and whites. A race-specific analysis has not 
been reported, but self-perceived level of physical activity exhibited a 
positive relationship to income. The likelihood of a direct association 
between nonwork-related physical activity and SES is also suggested by the 
results of a statewide Massachusetts Survey (probably predominantly white) in 
which reported participation in sports and exercise increased linearly with 
both education and income (45) . 

CHD Risk Factor Characteristics of Upwardly Mobile/High SES Blacks 

Two population samples examined within the last decade provide relatively 
complete data on CHD risk factors in blacks at the upper end of the SES 
spectrum. The Framinghara Minority Study (36) examined a random sample of 45 
black men and 55 black women, residing in Framinghara, Massachusetts in 1980. 
The educational characteristics and HDL-cholesterol data of this sample have 
already been discussed. The age range of the participants was 20-69 years and 
the mean age was 42 years for both sexes. A younger sample of blacks who may 
be upwardly mobile is represented by University of Pittsburgh freshmen 
recruited during the 1982-1983 and 1983-1984 academic years (46). This sample 
included 285 black students (134 men and 151 women; mean age of 18.0 +0.6 
years for each sex). Their parents were well-educated compared to the general 
black population. They represented a relatively homogeneous population with a 
median family income of $21,000 which is similar to $20,500 for the general 
white population, and far in excess of the $11,600 median income for the 
general black population. 

Mean blood pressures of Framinghara Minority subjects were considerably 
lower than those of the general U.S. population (47). However, the small 
sample size precludes definitive statements in this regard. The Pittsburgh 
freshmen had lower systolic blood pressures than those observed for men and 
women of comparable age in the First National Health and Nutrition Examination 
Survey (NHANES I) (47). In the Framinghara Minority Study, 13% of the men had 
hypertension and 18% of the women. In the Pittsburgh sample, 6.0% of the men 



292 



and 4.0% of the women had either SBP ^ I'^O ™" ^S °^ °BP ^ 90 mm Hg. 
Comparable figures are 15.0% for men and 3.2% for women ages 18-24 in the 
general U.S. population. 

The prevalence of cigarette smoking in the Fraraingham Minority study was 
42.2% for men and 30.9% for women. Comparble data reported in the NHANES II 
study were 46.5% and 29.9% for black men and women, respectively (41). This 
is similar to the prevalence of smoking in the U.S. white population but lower 
than that of U.S. blacks described in the NHANES I (48). Relatively few of 
the Pittsburgh Freshmen were smokers, 7.5% of men and 10.7% of women. 

Framingham Minority Study men had a mean body mass index similar to that 
of the U.S. general population. However, the 90th and 95th percentiles of 
body mass index for black Framingham women were somewhat lower than those of 
U.S. black women (49) suggesting a lower prevalence of obesity in this 
population and a greater similarity to the white female population. 

The HDL-cholesterol levels of the Pittsburgh black men were significantly 
greater than those of a white Pittsburgh freshmen comparison group (50). This 
reflected primarily differences in the HDL2 fraction. However, for women 
there was no difference in HDL levels between black and white Pittsburgh 
freshmen. In addition, self-reported physical activity levels paralleled the 
HDL-chol and HDL2-chol results. That is, black females and white females had 
similar self-reported physical activity levels while black males had a 
significantly higher self-reported activity level than white males (51). 

Socioeconomic Status and Cardiovascular Health Knowledge 

The data presented so far on associations of SES with behaviors which 
affect cardiovascular risk suggest that cigarette smoking is more likely among 
blacks of low-SES, and smoking cessation and high levels of regular leisure- 
time physical activity are more likely among blacks of high-SES. 

The few available studies of knowledge of cardiovascular risk factors 
among blacks suggest relative lack of knowledge among low-SES blacks regarding 
the association between certain dietary practices, including intake of salt 
and saturated fat, on cardiovascular risk profiles (52,53). A 1982 telephone 
survey of a national probability sample of 1000 subjects performed by the Food 
and Drug Administration and the National Heart, Lung and Blood Institute 
revealed that respondents who were poorly educated, of low income or resident 
in the South had less than average awareness of diet-health relationships. In 
particular, educational level was positively correlated with concern about 
consumption of fats and cholesterol. In addition, food purchasing, food 
preparation, and food consumption habits among low-SES blacks are intimately 
connected with a culture of poverty (54). 

The available data suggest the need for focused and behavioral ly-oriented 
cardiovascular health education programs in socioeconomically deprived black 
populations . 



293 



Conclusions 

There are limited data on the relationship between social class and 
cardiovascular disease incidence and mortality in blacks. However, these data 
suggest that the risk of coronary disease is higher among low-SES blacks than 
among high-SES blacks. The data on the relationship between SES and the 
prevalence of CHD risk factors in blacks also suggest an association of low- 
SES with higher prevalence of hypertension, obesity, and cigarette smoking. 
Since the excess prevalence of diabete.s in middle-aged black women appears to 
be related to obesity (55), this may reflect some influence of SES. High-SES 
appears to be associated with a lower prevalence of hypertension, a greater 
likelihood of smoking cessation, and greater leisure-time physical activity. 
Only in the case of HDL-cholesterol does there appear to be an association 
between high-SES and a potentially adverse level of the risk factor. 

No study to date has examined the impact of "upward mobility" 
(operationalized as described earlier) on CHD risk factors in blacks. In the 
case of HDL-cholesterol, this appears to be an important area for future 
investigation. If, as has been suggested, HDL-cholesterol might account for 
the lower CHD incidence in black men observed in some studies, it would be 
important to take explicit account of social class and social mobility 
differences among blacks in future cohort or surveillance studies. 

In addition, if socioeconomic improvement is associated with a lower 
incidence or prevalence of risk factors such as hypertension, obesity, 
diabetes mellitus, and cigarette smoking, it is conceivable that factors which 
impede such improvement among blacks might contribute to persistently higher 
levels of these risk factors than in whites. However, it is probably 
inappropriate to focus on economic factors to the exclusion of cultural 
factors. The recent (1979-1982) evaluation by Stern et al (56) of CHD risk 
factors among Mexican Americans in three San Antonio neighborhoods, (labelled 
"traditional", "transitional" and "suburban") revealed an inverse relationship 
between socioeconomic status and the "obesity-related" CHD risk factors, 
diabetes mellitus, hypertriglyceridemia and low HDL-cholesterol levels in 
women. Among men, such a relationship existed only for diabetes, and was less 
marked. On the other hand, total cholesterol levels and low density 
lipoprotein cholesterol levels were higher in more affluent men, but not in 
women. The observation that "obesity-related" risk factors were higher in 
Mexican Americans than in Anglos of similar SES in the same neighborhoods 
suggested that cultural factors might be more important than socioeconomic 
ones. Dietary, physical activity, cigarette smoking, and alcohol consumption 
habits are among the possible culturally-based determinants of CHD risk. 

The issue of socioeconomic and sociocultural change and its effect on CHD 
risk factors and CHD incidence is an important one for blacks. Research 
should be initiated in this area. Simultaneously, interventions should be 
directed to fostering the possible beneficial effects of socioeconomic and 
sociocultural change and blunting possible adverse effects. 



294 



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42. Covey LS, Mushinski MH, Wynder EL. Smoking Habits in a Hospitalized 
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120:834-851, 1984. 



299 



Coronary Heart Disease in 
Black Populations: Current 
Research, Treatment, and 
Prevention Needs 




Hector F. Myers, Ph.D. 

Department of Psychology 

University of California at Los Angeles 



ABSTRACT 



This paper summarizes the existing knowledge base contained in the 
collection of papers and reports from two national meetings on coronary 
heart disease (CHD) in black populations. Evidence is presented that 
suggests that CHD morbidity and mortality rates are roughly comparable 
between blacks and whites, but blacks appear to be at greater risk of 
sudden death than whites due to the higher prevalence of hypertension, 
obesity, diabetes, and greater socioeconomic disadvantage. The quality 
and availability of sound eoidemiologic data on CHD in blacks are 
generally criticized, and specific recommendations for improvements are 
offered. 

An extensive review of available evidence on risk factor status and 
trends in black and white populations is also provided, and speculations 
about possible racial differences in operative risk factors and 
function, and in protective factors are made. Arguments are provided 
for the salience of socioeconomic and sociocultural factors in CHD In 
blacks, and an analysis of how these factors might interact to affect 
CHD risk status, risk management, and CHD morbidity and mortality 
differences is offered. 

Consideration of the possible role of differences in the quality, 
effectiveness, and accessibility of health care between blacks and 
whites as possible contributors to the observed CHD differences is 
given. Provocative evidence of differential patterns of medical care of 
CHD patients as a function of race and socioeconomic status is 
presented. 

Finally, the need to support CHD prevention activities is 
discussed, and specific programmatic recommendations for future research 
on coronary heart disease in black populations are offered. 



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INTRODUCTION 

The American Heart Journal recently nublished a SDecial supplement 
issue that compiled the papers and plenary group reports from two 
national meetings on coronary heart disease in black populations: a 
symposium sponsored by the American Heart Association Council on 
Epidemiology, and a working conference sponsored by the National Heart, 
Lung, and Blood Institute (NHLBI) (American Heart Journal (AHJ), Sept., 
1984, Vol. 108, No. 3, Part 2). These meetings and the subsequent 
publication were catalyzed by the recommendations of the Black Health 
Care Providers Task Force on High Blood Pressure Education and Control 
(BHCPTF) and by the recent publication of two major review papers on 
coronary heart disease in blacks (Gillum, 1982; Gillum & Grant, 1982). 
Both factors stimulated the interest and concern of medical and social 
scientists in exploring the range of issues and questions raised about 
coronary heart disease in black populations. 

To this end, the papers in the special AHJ issue reviewed and 
discussed the major theoretical and clinical issues regarding the 
incidence and prevalence of CHD, the operative risk factors for CHD, and 
the possible contributory role of current medical attitudes and 
practices in CHD-related deaths among blacks. The working conference 
participants also offered a series of specific recommendations for 
further research needs and priorities. This report provides an 
integrative summary of the state of our current knowledge about CHD in 
blacks as reviewed in the AHJ proceedings, and organizes the suggested 
research priorities into coherent programmatic recommendations to guide 
future research on coronary heart disease in this population. 

Four major substantive questions emerge as salient concerns in the 
recent reviews on CHD in black populations. First, what conclusions can 
be drawn from our present epidemiologic evidence on the incidence and 
prevalence of coronary heart disease in black Americans as compared to 
white Americans? Included here are considerations of CHD morbidity and 
mortality, and sudden death, as well as epidemiologic and other evidence 
on angina pectoris, myocardial infarction (MI), and coronary 
atherosclerosis as integral to the CHD spectrum. 

The second major question is: What are the specific risk factors 
and possible resistant or protective factors for CHD for blacks, and to 
what extent do blacks and whites differ in the nature and relative 
importance of these factors? Consideration is given here to whether or 
not the CHD risk factors identified for whites are the same and have the 
same degree of importance for blacks, and whether there may be genetic 
and/or socioenvironmental factors that increase the resistance of blacks 
to coronary heart disease. 

The third major question is: What role do socioeconomic, 
sociopsychological , and sociocultural factors play in the observed 
patterns of CHD morbidity and mortality in blacks? Consideration is 
given here to the range of social factors that exert detrimental 
effects on the social and health status of black Americans. Particular 
attention is paid to the conceptualization and measurement of these 
factors, as well as to the specification of their differential imoact on 



304 



CHD risk and risk management, on CHD morbidity, on medical treatment of 
CHD, and, ultimately, on CHD mortality in blacks. 

The fourth major question addresses the health care system. 
Specifically, to what extent do physicians' attitudes and beliefs, and 
clinical practices in health-care institutions in treating coronary 
heart disease in blacks result in either differential access or 
differential quality of medical care for blacks? Furthermore, to what 
extent do these practices ultimately contribute to the 
disproportionately higher MI case fatality rates for blacks? 



CONCEPTUAL PERSPECTIVE 

Underlying these major concerns about CHD in black populations is a 
conception of hypothesized roles that various factors play in 
determining risk for CHD, in impacting on the course of the disease, and 
ultimately on the outcome of this disease in black populations. 
Included are biological factors, and psychosocial and sociocultural 
factors, all of which interact to differing degrees and at different 
points in the coronary heart disease process. 

Current conceptual models confer priority on biologic processes 
(i.e., genetic and metabolic) and on health behaviors as primary 
contributors to CHD risk, morbidity, and mortality. A family history of 
high blood pressure or of CHD, elevated blood pressure, presence of ECG 
abnormalities, obesity, diabetes, and high cholesterol levels are all 
acknowledged biologic risk factors. Similarly, personal health habits 
including smoking, limited physical exercise, heavy alcohol consumption, 
and such psychosocial factors as disadvantaged socioeconomic status, 
sustained disturbing emotions (e.g., anger), a time-oressured, 
aggressive behavioral type (Type A), and high life stresses have all 
been associated with increased CHD risk (Figure 1, Kasl , 1984; McDonald 
et al., 1984; Gillum & Grant, 1982). Finally, a tendency to ignore, 
deny, or minimize the significance of CHD symptoms (e.g., chest pains), 
and to delay seeking medical care has also been associated with 
increased risk for CHD-relffted deaths (Gillum, 1982). 

These factors are viewed as interacting to affect CHD morbidity, 
with the psychosocial factors operating primarily as mediators of the 
biological predispositions. However, several questions have been raised 
about whether some of the psychosocial factors might not operate as 
independent precursors. Smoking has been identified as an accepted risk 
factor for CHD and there is preliminary evidence that Type A behavior is 
a potential risk factor for CHD; these are examples of factors that 
operate biobehaviorally to increase CHD risk (Kleinman et al . , 1979; 
Coronary Prone Behavior Review Panel, 1981). Similarly, questions have 
been raised about socioeconomic disadvantage which appears to be a 
social system precursor of a variety of pathogenic outcomes including 
CHD (James, 1984a). 

In addition to their direct and indirect effect on CHD risk, 
psychosocial factors also seem to affect disease course by influencing 
risk behavior management and the recognition and management of symptoms. 



305 



This is particularly true of such factors as socioeconomic status, 
cultural beliefs about health and illness, symptom tolerance, healinn 
beliefs and practices, and help-seeking behaviors (Jackson, 1981). 
Individual help-seeking behavior, compliance behaviors, and attitudes 
toward the sick role also contribute to the course of CHD. 

Symptom recognition and management are also likely to be affected 
by the prevailing beliefs and treatment practices of health care 
providers. These include the knowledge and beliefs of individual 
physicians about CHD in particular populations, the pattern of usual 
care provided to CHD victims (e.g., diagnostic and treatment practices), 
and the host of factors that affect the pattern of care likely to be 
provided (e.g., financial resources of the patients, the technical 
resources of the providers, etc.) (Davis et al., 1981; Yelin et al . , 
1983; Brook et al . , 1983). Analyses of health care system factors 
should also include the availability and response times of emergency 
services, and the beliefs and behaviors of these personnel when 
responding to CHD crises in low-income, black communities. Although 
comparatively less is known about the contribution of health care system 
factors in CHD morbidity and mortality, there is preliminary evidence 
suggesting that certain patient characteristics such as race, ability to 
pay, gender, and age may contribute to differences in the quality of 
medical care received, and to the pattern of health compliance behaviors 
observed (Shapiro et al . , 1970; Jackson, 1981; Yelin et al . , 1983). 
This interaction of differential treatment and differential pre- and 
post-hospital patient behaviors probably contributes ultimately to 
differential CHD mortality rates in the affected groups. 

In sum, at the core of our concerns about CHD in black populations 
is the need to identify the ma.ior biologic, sociopsychologic, 
sociocultural , and health care system factors that may be causally 
implicated in this disease. There is a related need to specify more 
carefully to what degree and at what point in the CHD process these 
factors make their contributions, and whether the contributions are 
direct or indirect. In the specific case of CHD in blacks, we must 
actively entertain the possibility that not only is the pattern of 
occurrence of CHD somewhat different, but that the factors causally 
implicated and their pattern of contribution at each point in the CHD 
process in blacks may differ significantly from that reported for 
whites. The justification for this hypothesis rests in the suggestive 
evidence reported in the most recent review on CHD risk factors (Curry 
et al., 1984; Tyroler, 1984; McDonald et al., 1984). 



WHAT DO WE PRESENTLY KNOW ABOUT CHD IN BLACKS? 

1. Epidemiologic Evidence 

There is general consensus that our present epidemiologic data on 
coronary heart disease in blacks are inadequate. Specific criticisms 
have been levelled at the practice of the National Center for Health 
Statistics and other national health data collection agencies of 
collapsing all health statistics on blacks into the "non-white" 
category. This practice confounds the health trends of the various 



306 



ethnic minoritips and, in so doing, obscures important differences 
between them. The national health surveys such as the National Health 
and Nutrition Examination Surveys (NHANES) I and II, and some of the 
major cardiovascular disease surveillance and treatment studies, when 
they have not excluded blacks from their samples (as in the Framingham 
Heart Study), have used small, nonrepresentative samples — inadequate 
indicators of national black population trends. In the Multiple Risk 
Factor Intervention Trial (MRFIT), for example, only 6.5% of their 
randomized sample was black. In the Hypertension Detection and 
Follow-up Program (HDFP), however, the investigators, recognizing the 
importance of hypertension in the black population, oversampled and thus 
enrolled a sample that was 26% black, in the study, as a whole. In the 
hypertensive group of HDFP, 44% were black. Questions have also been 
raised about how representative the largely rural, southern, black 
samples in the Evans County and Charleston Heart Studies are of black 
populations elsewhere in the nation. 

Several investigators have also questioned the scientific basis for 
our rather simplistic classification of groups by race, the tendency of 
many to infer (inappropriately) that observed racial grouD differences 
are due to biologic differences between the groups (Cooper, 1984), and 
the tendency of many biomedical investigators to ignore the biologic, 
socioeconomic, and psychosocial heterogeneity of blacks (Watkins, 1984a; 
James, 1984a, b; Myers, 1982). Our present knowledge sunqests that the 
U.S. black population is neither biologically nor socioeconomically 
homogeneous and, as such, failure to take adequate account of this 
heterogeneity in study samples is likely to produce nongeneralizable 
findings, or may result in incorrect conclusions about the contribution 
and significance of race as a biologic factor in explanations of 
observed differences between blacks and whites. This error of assuming 
homogeneity in study cohorts is probably also committed with respect to 
whites and other ethnic groups. 

As a result of these conceptual and methodologic problems, there 
are ongoing disagreements about what conclusions can be drawn about 
coronary heart disease prevalence and mortality rates, and about the 
incidence of myocardial infarction in blacks. Gillum (1982) and Watkins 
(1984a) both note contradictory findings when comparing vital statistics 
with mortality data from more carefully designed epidemiologic studies 
that included large samples of blacks. For example, according to the 
vital statistics, the age-adjusted mortality rates from CHD in blacks 
exceeded those of whites, especially between the age-groups 35-44 years, 
45-55 years, and 55-64 years. Similarly, the CHD mortality rate for 
black women exceeds that for white women (Report of the Working Group on 
Atherosclerosis, 1981). However, when these data are compared with the 
mortality rates from the MRFIT screenee population, the American Cancer 
Society (ACS), and the Evans County studies, the CHD mortality rates for 
black men range from 78% to 90% that of white men. Only the excess CHD 
mortality rate for black females (i.e., 107% in the ACS study) is 
consistent with the national mortality data. 

This picture is further complicated when the data on sudden death 
are considered. The results of the Charleston Heart Study show that, 
between 1960-1975, black males were three times and black females 1.5 



307 



times more likely to die suddenly (i.e., within 1 hour of onset of 
symptoms) than were white males and females (Keil et al . , 1984). On the 
other hand, the Baltimore sudden death study revealed no black-white 
differences in sudden death (Kuller, Perper & Cooper, 1975). Questions 
were raised by Watkins (1984a) about whether these contradictory 
findings are due to differences in death certification and/or to 
differences in access to medical care. 

Although many studies also report a lower prevalence of CHD in 
blacks, other studies report that younger blacks and black women show 
evidence of more CHD symptoms than do whites (Gillum, 1982; Langford et 
al., 1984). Among MRFIT screenees followed for 5 years, blacks appeared 
to be at greater risk for cerebrovascular accidents than whites, given 
the higher overall prevalence of essential hypertension (Neaton et al., 
1984) and, in the Charleston Heart Study, blacks had a higher MI 
case-fatality rate than their white counterparts (Table 2, Keil et al . , 
1984). Furthermore, although CHD-related mortality has decreased 
significantly in both blacks and whites since 1968, there is still a 
large disparity in black-white CHD mortality rates because of the 
persisting excess CHD mortality rates for black females (Figure 1, 
Gillum & Liu, 1984). Important age, gender, socioeconomic status, and 
geographic differences are also evident and must be considered in 
interpreting these findings (Gillum & Liu, 1984; Savage et al . , 1984; 
Watkins, 1984a; Figures 1-4, Leaverton et al., 1984; Strong et al., 
1984; Keil et al . , 1984). 

These somewhat contradictory findings, along with the limited data 
sources and the methodological limitations of many of the studies 
reviewed, make it unwise to draw firm conclusions about the true 
prevalence of CHD and its consequences in black populations. However, 
it is clear that CHD is far from uncommon among blacks, and that blacks 
are not immune to its effects. Rather, what we see is preliminary 
evidence of gender differences in the pattern of CHD morbidity and 
mortality when different races are compared. For example, if we look at 
overall CHD mortality rates, then both black and white men have 
significantly higher rates than both black and white women, but black 
women have significantly higher mortality rates than white women (Figure 

1, Gillum & Liu, 1984). On the other hand, if we consider sudden death 
rates, than black men and women appear to be at greater risk than their 
white counterparts (Gillum, 1982; Keil et al . , 1984). 

2. Risk Factor Differences 

Several hypotheses have been proposed to explain the possible 
reasons for these racial differences in CHD. The two most promising 
hypotheses are (1) that there are racial differences in the operative 
risk factors for CHD, and (2) that blacks may have some biologic and/or 
psychosocial protective factors which may reduce their CHD risk. An 
alternative hypothesis is that the standard CHD risk factors may be of 
different degree of importance (i.e., different risk functions) (Curry 
et al., 1984; Table 4, Figures 4 & 5, Tyroler, 1984; McDonald et al . , 
1984). The available evidence also identifies several differences 
between blacks and whites such as in the prevalence of hypertension, in 
metabolic or biochemical factors, and in psychosocial characteristics 



308 



that suggest that different factors may potentiate coronary heart 
disease in these group. 

a. Biological Risk Factors 

A strong family history of coronary heart disease is an 
accepted risk factor for both blacks and whites. However, a family 
history of essential hypertension may not be as strong a predictor of 
coronary heart disease for blacks given the greater overall prevalence 
of hypertension in black populations (Curry et al., 1984; Neatnn et al., 
1984). For example, in the five-year follow-up of 361,620 men screened 
for the MRFIT study, although elevated blood pressure was a strong 
predictor of CHD mortality in whites, high blood pressure appeared to be 
a better predictor of cerebrovascular disease and CVD mortality than of 
CHD mortality in these black men (Neaton et al . , 1984). This does not 
mean, however, that hypertension in blacks is not a major CHD risk 
factor. The evidence is incontrovertible that there is a high 
population-attributable risk of hypertension for all-cause mortality and 
for CHD mortality in blacks (See Table ?. and Figure 1, Tyroler et al . , 
1984; Figures 1 & 2, Neaton et al., 1984; Haywood, 1984)". For these 
reasons, aggressive prevention and treatment of hypertension must be 
continued (Tyroler, 1984). 

Similarly, the presence of such ECG abnormalities as minor S-T 
segment depressions and T-wave abnormalities may not have the same 
diagnostic significance for blacks as for whites (Bartel et al . , 1971) 
given the greater prevalence of these abnormalities in elderly U.S. 
black populations (Riley et al., 1973) and even in black societies 
in Africa and the Caribbean (Watkins, 1984b) where there is low CHD 
prevalence. However, when abnormalities indicative of left ventricular 
hypertrophy (LVH) are present in conjunction with other major risk 
factors, then total mortality risk is likely to be even higher for 
blacks than for whites (Table 1, Tyroler, 1984). 

On the other hand, obesity and diabetes mellitus, which are not as 
prevalent among whites, may be more significant risk factors for CHD 
among blacks, especially for black women (Curry et al . , 1984; Tables 6 & 
7, Cooper et al . , 1984;' McDonald et al . , 1984). For lipid profiles, the 
situation is somewhat more complex. Typically, blacks tend to have 
higher HDL-cholesterol (HDL = high-density lipoprotein) and 
apolipoprotein Al levels, and Tower levels of LDL-cholesterol (LDL = 
low-density lipoprotein), VLDL-cholesterol (VLDL = "^^ry low-density 
lipoprotein), apolipoprotein CII, and triglycerides than whites 
(Gartside et al . , 1984; Figures 1-4, Glueck et al., 1984; Figures 3-5, 
Heiss et al., 1984; Rowland & Fulwood, 1984; Neaton et al., 1984), This 
combination of higher HDL- and lower LDL-cholesterol levels for 
equivalent total cholesterol level may confer some protection on blacks. 
Unfortunately, there is some preliminary evidence from the MRFIT study 
suggesting that an unexpected by-product of aggressive 
pharmacotherapeutic intervention in hypertension is a significant 
reduction in HDL-cholesterol level especially when propranolol is added 
to diuretic regimens. Concurrent changes in diet and weight may have 
also contributed to these changes in the lipoproteins (Lasser et al . , 
1984; Curry et al . , 1984). Tyroler (1984), however, argues against 



309 



overinterpretinq these results as directly relevant to the larqe 
population of black hypertensives, since these findings were obtained in 
a select sample of upper middle-class white men. Whatever reduction, if 
any, in degree of protection against CHD that may result from diuretic- 
and propranolol-induced HDL-cholesterol level changes is not comparable 
in magnitude to the significant benefits derived from aggressive blood 
pressure control in black communities. 

McDonald et al . (1984) also point to several apparent biochemical 
risk factor differences between blacks and whites that include 
differences in sodium/potassium ratios in urine, in plasma renin and 
epinephrine levels, in hematocrit values, in differential rates of G6PD 
enzyme deficiency, and in possible differences in transport of these 
electrolytes via the sodium/potassium pump in the red blood cells. All 
of these differences may be related to blood pressure differences 
between the groups. However, as noted by Watkins (in press), the Evans 
County, Georgia study found that black-white differences in blood 
pressure were not due to higher sodium intake in blacks (Grim et al., 
1980). Blaustein (1984) and Trevisan et al. (1984) also discount 
disturbances in the sodium transport mechanism as accounting for racial 
differences in hypertensive populations. 

b. Psychosocial Risk Factors 

When we consider the host of psychosocial risk factors 
implicated in coronary heart disease, the picture is even more complex.. 
Psychosocial risk factors for CHD that are generally accepted or 
suggested include cigarette smoking and heavy alcohol consumption, 
social isolation and inadequate social support, and sustained disturbing 
emotions (e.g., anxiety, hostility, etc.), especially as part of the 
Type A behavior pattern (Coronarv Prone Behavior Review Panel, 1981; 
McDonald et al., 1984). 

In the case of blacks, these factors do not appear to ooerate as 
directly or to have the same demonstrated importance as they do for 
whites. For example, socioeconomic disadvantage, including experiences 
of racism and discrimination, appears to make a more significant risk 
contribution for blacks than for whites (Tyroler et al., 1984; James, 
1984a). On the other hand, risk behaviors such as smoking, alcohol 
consumption, and limited physical activity appear to be pathogenic to 
blacks and whites to the same degree. However, although more blacks 
smoke, black smokers typically smoke fewer cigarettes than white smokers 
(See Table 6, Garfinkel, 1984). Similarly, the relationship between 
cigarette smoking and pattern of CHD and risk appears to be different 
for blacks and whites. Neaton et al . (1984) note that, in the MRFIT 
screenee follow-up studies, different 5-year, age-adjusted, CHD 
mortality rates were obtained for black and white men as a function of 
the number of cigarettes smoked (Figure 8). They also noted that black, 
5-year, cerebrovascular mortality rates were significantly higher than 
for whites, for a comparable number of cigarettes smoked (Figure 9). 

In addition, there are complex interrelationships between cigarette 
smoking, cholesterol levels, and blood pressure that impact on CHD 
mortality; these appear to be discordant between blacks and whites 



310 



(Neaton et al., 1984; Garfinkel, 1984). The relative risk (RR) of CHD 
death over 5 years, in smokers compared to nonsmokers, was relatively 
constant in subgroups of black and white MRFIT screenees categorized 
according to serum cholesterol level (250 mg/dl ) and diastolic blood 
pressure (DBF), both^90 mm Hg and<90 mm Hg. The RRs lay in the range 
1.62 - 1.83. In contrast, for men with a serum cholesterol level of 250 
mg/dl, the corresponding RRs lay in the range 2.23 - 3.72, and were 
highest for black males with a DBF of 90 mm Ha (RR = 3.72) and for white 
males with a DBP of 90 mm Hg (RR - 2.87). However, the highest 
mortality rates were observed among smokers with elevated serum 
cholesterol levels, in black normotensive men, and in white hypertensive 
men (Table 7, Neaton et al., 1984). 

Also, blacks as a group tend to be more physically active than 
whites (Rowland & Fulton, 1984), although this difference may well be 
due to socioeconomic status-related differences in the proportion of 
white- vs. blue-collar workers in these groups. 

Research on the role of Type A behavior pattern and related effects 
of strong emotions on CHD risk, although extensive for whites (Review 
Panel, 1981) is extremely limited for blacks (James, 1984b). The 
absence of relevant research on this Question is a major lacuna in the 
literature. The related work on suppressed anger (Diamond, 1983) and, 
most recently, on the interaction of low education and the John 
Henry- type coping pattern in hypertensive black men (James, 1984c) 
suggests that these psychological processes need to be seriously 
considered as possible risk factors in CHD in blacks as v/ell. Similar 
attention should be given to occupational stresses (House, 1974; James 
et al., 1984d), and to social mobility (Gillum & Paffenbarger, 1978) as 
additional, potential risk factors for CHD, especially given thp unigue 
pressures faced by increasing numbers of black men and women who are 
entering professional and managerial occupations. 

At the broader socioecologic level, blacks face disproportionately 
greater CHD risks due to higher life stresses (Harburg et al . , 1973) and 
to lower medical care access, utilization, and, possibly, lower quality 
care (Yelin, Kramer & Epstefn, 1983). 

In addition to the consideration of risk factors, there is also the 
need to explore the role of possible biologic and psychosocial 
protectors against CHD. Given 'the higher prevalence of hypertension and 
comparable prevalence of other CHD risk factors in blacks, it is 
surprising that the prevalence of CHD and CHD mortality rates in blacks 
is not even higher (Gillum, 1982). One possible explanation for the 
current lower-than-expected rates in blacks is the presence of factors 
that confer some degree of protection against CHD on blacks. We have 
already reviewed the evidence of possible biologic protection in the 
lipid profile that combines higher HDL-cholesterol and apolipoprotein Al 
levels with total cholesterol level, which is more common in blacks than 
in whites (Heiss et al . , 1984; Glueck et al., 1984). It would also be 
useful to explore the possible protective role that social supports 
(Broadhead et al . , 1983), psychological hardiness (Kobasa, Maddi & Kahn, 
1982), a high sense of personal, social, and cultural coherencp 
(Antonovski, 1979), low "John Henryism" (James et al . , 1984c), and other 



311 



adaptive stress-coping styles (Billings & Moos, 1981) may olay in 
reducing CHD risk in blacks. 

In sum, these data point to the need to pursue actively this 
question of possible racial differences in CHD risk factor levels and 
risk functions, as well as in protective factors. In this process, a 
multidimensional perspective that includes biological, psychological, 
and social risks, as well as possible protectors, should be considered. 

3. The Salience of Socioeconomic & Sociocultural Factors 

A major recurrent theme in the debate over black/white differences 
in the pathogenesis of coronary heart disease is the apparent 
differential significance of socioeconomic status (SES) and 
sociocultural factors. There seems to be some consensus of opinion 
that, for blacks, social status and related sociocultural influences 
probably contribute in some as-yet-undefined way to the observed pattern 
of CHD risks and outcomes (Myers et al . , 1984; James, 1984a, b; Kasl, 
1984). This consensus appears to be based on a collection of 
theoretical formulations, clinical observations, and on provocative 
empirical evidence. The absence of more conclusive data seems to be due 
to deficits in the conceptualization, specification, and measurement of 
social status variables; to inconsistencies in the consideration of 
these variables in studies of CHD; and to the frequent omission of these 
variables, or to the confounding of these variables, with race in 
studies of CHD in multiethnic populations. A related ooint is that 
investigators typically look for main effects of SES and related 
variables rather than testing the hypothesis that these factors may 
operate interactively with other factors. The hypothesis that these 
variables may be important to different degrees in different 
populations, and may operate at different points in the CHD process is 
also typically ignored. 

An alternative conceptualization of social status and of this 
selective effects' hypothesis was articulated in the Working Group III 
report (Myers et al., 1984). The contributors suggested that 
socioeconomic and sociocultural factors should be subsumed under the 
generic heading of social status, and that this construct should be 
defined multidimensionally. Sociostructural and sociopsychological 
characteristics were distinguished and speculations about their 
contributions to CHD were made. Sociostructural features of social 
status include such factors as race, education, occupation, income, 
marital status, and social mobility. These factors define social status 
through the social meanings, institutions, and practices that govern 
life opportunities and obstacles for blacks. The sociopsychological 
features of social status, on the other hand, include the host of 
individual differences in experiences and personal attributes, 
resources, and liabilities, all of which determine individual 
vulnerability or resistance to objective external social conditions. 
These include personality characteristics, life stresses, coping styles, 
the availability and use of social supports, patterns of help-seeking, 
and characteristic levels of anxiety, happiness, anger, and other 
similarly strong emotions. 



312 



In the assessment of these factors, careful attention must be given 
to distinguishing objective, concrete events and experiences that blacks 
face from the subjective interpretations and meanings conferred on these 
experiences. The latter include consideration of both individual and 
collective group meanings (McDonald et al., 1984; James, 1984a; Kasl, 
1984; Myers, 1982). 

In addition, consideration should be given to the analysis of main 
effects and interactions of social status as predictors of CHD outcomes. 
Most of the available evidence seems to provide more support for an 
interactional contribution of these variables toward predicting illness 
outcomes (Harburg et al., 1973; Kasl, 1984). 

Finally, there is growing justification for considering separately 
the influence of social status on the presence of factors that either 
increase or decrease CHD risk status; on factors that influence the 
management of risk (i.e., early symptom identification, intervention, 
and disease prevention); on factors that influence the level of CHD 
morbidity observed; and on factors that ultimately affect the level and 
pattern of CHD mortality observed in the black population. Social 
status factors may also exert their impact through such health care 
system factors as the timing and availability of medical services, the 
accuracy of clinical diagnosis, and the appropriateness and 
effectiveness of the treatment received (Myers et al . , 1984; Cooper et 
al., 1981; James, 1984a; Kasl, 1984). Figure 1 in Myers et al . (1984) 
describes these hypothesized influences in a simplified diagram. 

4. Racial Differences in the Diagnosis, Treatment, & Course of 
Coronary Heart Disease 

The final substantive concern is whether the observed black/white 
differences in CHD mortality might be due, in part, to differences in 
the natural history and treatment of CHD. This concern over possible 
differential health care system effects as a function of race and social 
class is based on anecdotal, clinical, and preliminary research reports 
that suggest that there are important differences between blacks and 
whites in rates of access and utilization of preventive and emergency 
medical services (Jackson, 1981; Yelin et al . , 1983). Also, reports of 
differences in risk status at the point at which treatment is initiated 
(Haywood, 1984a, b; Francis et al . , 1984; Curry et al . , 1984), and 
differential use of coronary arteriographic and coronary artery bypass 
grafting (CABG) procedures with black and white CHD patients (Oberman & 
Cutter, 1984) have been noted. Physicians have also reported greater 
resistance to, and lower compliance with, medical regimens among black 
patients: This is believed to contribute toward diminishing the 
effectiveness of treatment (Jackson, 1981). Data are inadequate with 
respect to secondary prevention efforts (Oberman & Cutter, 1984), but 
those studies that used standardized diagnostic and intervention 
procedures (e.g., MRFIT & HDFP) show that blacks often derive similar or 
greater benefit than whites from such intensive approaches to CHD risk 
reduction and treatment (Tables 6 & 7, Rowland & Fulwood, 1984; Table 5, 
Connett & Stamler, 1984; Table 5, Langford et al . , 1984). 



313 



The data on surgical outcomes for black CHD patients are also 
inadequate (Haywood, 1984). However, preliminary evidence suqgests that 
blacks show no greater operative mortality risk to myocardial 
revascularization procedures when hypertension, diabetes, and prevalence 
of hyperlipidemia are taken into account (Table I, Sterling et al., 
1984). 

It is apparent from these reviews that no strong conclusions about 
black/white differences in the natural course of CHD are justified at 
this time, given the paucity of good data. However, there is enough 
evidence to justify the suspicion that some racial and SES differences 
in CHD course do exist, and that these differences are probably 
attributable to differences in level of risk, pattern of health care 
utilization, and in the pattern of health care system characteristics. 
These factors probably interact to produce a more pathogenic process, 
high CHD mortality, and higher CHD-related sudden death rates in black 
Americans. 



RECOMMENDATIONS FOR FUTURE RESEARCH 

The present evidence supports the contention of Gillum and others 
(Gillum, 1982a; Gillum & Grant, 1982) that CHD is a major health problem 
for black Americans. Further, though there is growing and provocative 
evidence suggesting that blacks and whites may not differ significantly 
in overall prevalence and incidence rates for CHD, these groups do 
appear to differ in overall CHD mortality and sudden death rates. 
Furthermore, low-income blacks, and black women in particular, appear to 
be at greater mortality risk than their male, white, and upper-SES 
counterparts. In addition, the evidence suggests that many of these 
racial differences may well be due to differences in biologic and 
psychosocial risk factors, as well as to differences in the usual 
diagnostic and treatment practices for suspected CHD. 

Because of such significant deficits in the available data on CHD 
in blacks, these statements should be treated as tentative and viewed 
more as interesting hypotheses to be pursued vigorously rather than as 
firm conclusions. The significance of these issues to the health of the 
nation, however, clearly justifies an aggressive approach toward 
answering major questions about CHD in black populations. The chief 
areas of deficit and the appropriate recommendations for future research 
are organized programmatically as follows: 

1. The most glaring lacuna results from the limited availability 
of epidemiologic and clinical data on CHD in blacks. This 
deficit can be corrected by a two-stage process consisting of: 

a. first, existing NCHS data bases should be improved by 
separating the data on blacks from the "non-white" 
category, and by including large, nationally 
representative samples of blacks in all existing or 
proposed national health studies (e.g., NHANES, the 
Coronary Artery Risk Development Study, and the Community 
CHD Surveillance Studies); and 



314 



b. second, pnpulation-based prospective studies of black 
cohorts similar to the Framingham Heart Study should be 
funded. 

In all of these studies great care should be exercised in the 
selection of appropriately representative black samples, with 
consideration given to such sources of group variability as urban vs. 
rural residency, geographic location, socioeconomic status, and national 
origin. The reliability and appropriateness of the assessment and 
diagnostic tools and procedures used with this population must be 
demonstrated. 

2. The second major research priority should be a series of 

studies addressing the issue of differential CHD risk pattern 
and functions in blacks and whites. This priority could be 
addressed by: 

a. a more complete risk profile analysis of the black 
participants of the HDFP and MRFIT studies should be 
supported. This is a cost-effective strategy that avoids 
the high start-up costs typically associated with new 
research efforts with large samples; and 

b. the development of multi-center, multi-disciplinary, 
case-control studies focused specifically on such issues 
as sudden death in the community, hospital admission and 
discharge of patients with diagnoses compatible with CHD, 
emergency room visits for chest pain and related 
complaints, and surveillance of the offspring of indexed 
cases should be supported. The latter is probably more 
cost-effective than separate studies, and would take 
better advantage of existing research teams in 
geographically diverse areas with access to different 
black populations. 

Risk factor studies should be based on a multifactorial, biobehavioral 
perspective that includes possible biological, psychological, 
behavioral, and social sources of differences in risk factors and 
protective factors. Consideration of possible differences in both risk 
factor level and risk function should also be included. 

3. Finally, there is considerable justification for supporting studies 
that address the interface of patient and community characteristics on 
the one hand, and health care system characteristics and practices on 
the other, as predictors of CHD risk, natural course, and outcome. 
Priority should be placed on studies that focus on physician beliefs and 
attitudes, and the usual diagnostic and intervention practices used to 
treat black patients with suspected or confirmed CHD. Attention should 
also be given to how social status and associated sociopsychologic 
factors influence the host of CHD-related health beliefs and behaviors 
of blacks and how these, in turn, interact with the characteristics of 
community health care providers to affect the observed pattern of 
coronary heart disease morbidity, natural course, and mortality in black 



315 



populations. (See Appendix for a sumnary list of the specific research 
recommendations made). 

Underlyinq all of these recommendations is the need to give 
priority to sound conceptualization and methodological rigor. Most 
studies on CHD in blacks, as previously noted, suffer from a variety of 
conceptual and methodological deficiencies which must be avoided in 
future studies. Central among these are problems in the specification 
and adequacy of measurement of the variables of interest, and inadequate 
size and representativeness of the sample of blacks studied. Particular 
attention to the issues of socioeconomic status and to gender must be 
given in all of these studies. 

In addition to aggressive support for research on the causes of CHD 
in blacks, there is need also to increase support for prevention efforts 
directed at reducing CHD risk factors in blacks. Ultimately, little 
will be gained by knowing how prevalent CHD is in black populations or 
what factors contribute to its occurrence if we do not also act 
aggressively to prevent it. Results from the NHANES I 1^ II studies 
(Rowland & Fullwood, 1984), from the HDFP study (Langford et al., 1984), 
and from the MRFIT study (Connett & Stamler, 1984) show significant 
reductions in CHD risk-related factors in blacks through aggressive 
programs of education and treatment. Such efforts must be continued and 
should include greater black representation in future samples. 

In sum, the present evidence points to the significance of CHD as a 
major health problem for black Americans. Further, these data argue for 
the need for more aggressive and focused support for studies targeted at 
the major questions about CHD epidemiology, risk status, and 
patient-health care system transactions that might account for the 
observed CHD differences between black and white populations. Support 
for targeted primary prevention programs in black populations is also 
justified. 



This paper was prepared under personal services contract No. 263SGX13736 
from the Secretary's Task Force on Black and Minority Health, Department 
of Health and Human Services. Dr. Myers is also a Scholar-In-Residence 
at the Fanon Research & Development Center, Charles R. Drew Postgraduate 
Medical School, Los Angeles. The author wishes to express his 
appreciation to Dr. Laurence 0. Watkins and Elisabeth Pitt for their 
careful review and suggested revisions. 



316 



APPENDIX 



SUMMARY RECOMMENDATIONS FROM: 

The National Heart, Lunq, and Blood Institute's 
Working Conference on Coronary Heart Disease in Black Populations 

Bethesda, Maryland 
September 29-30, 1983 



PURPOSE: To review current knowledge about coronary heart disease in 
blacks and identify areas for priority research effort. The 
areas recommended included: 

• Prospective studies of the incidence of coronary heart disease in 
blacks. 

• Research to determine why black women apparently have higher 
coronary heart disease mortality rates than white women. 

• Research to determine the impact of antihypertensive treatment on 
coronary heart disease in blacks. 

• Research on ways to modify, in school-age populations, the 
development of eating patterns and physical activity behavior that 
may result in obesity in later life. 

• Research on variables such as risk factor patterns associated with 
coronary heart disease treatment, including coronary artery bypass 
surgery and angioplasty and its outcome in blacks compared with 
whites. 

• Studies of beliefs, awareness, and pre-hospital behavior that might 
delay appropriate diagnosis and treatment for individuals in the 
black community who hav^e symptoms of coronary heart disease. 

• Studies of risk factors for coronary heart disease in blacks that 
include investigation of the impact of socioeconomic status and 
ethnic diversity. 

• Special efforts be made to aid minority researchers and those in 
minority research settings to be competitive in seeking research 
funding. 



317 



SUMMARY RECOMMENDATIONS FROM: 

The National Heart, Lunq, and Blood Institute's 
Working Group to Discuss Strategies for Minimizing Coronary Heart 

Disease in Black Populations 

February 21-22, 1984 



PURPOSE: To develop research strategies to answer priority issues 

related to the gaps in our knowledge concerning coronary heart 
disease in blacks. 

Five task groups were convened to focus on priority issues 
developed by the previous conference. 

Task Group I focused on the problem of a paucity of epidemiologic 
data available on the occurrence of coronary heart disease among 
blacks and on the uncertain quality of mortality and morbidity data 
available for blacks . 

• They recommended further development of NHLBI research in 
community and cohort surveillance of coronary heart disease 
risk factors and events in black Americans. 

• They recommended a specific, prospective, community-based 
cohort study with oversampling of blacks in one geographic 
area which would ensure an adequate number and diversity of 
blacks to assess prevalence of coronary heart disease, and 
Dhysiologic and psychosocial risk factors of coronary heart 
disease. 

• Longitudinal follow-up for at least five years would then 
provide natural history data for an adequate number of blacks. 
The Task Group suggested that cooperation with the NHANES III 
study (to be carried out by the National Center for Health 
Statistics) would be desirable. The phase one validation and 
pilot studies, the definitive study, and the final data 
analysis would require an estimated eight years. 

• In addition, they recommended cohort studies among black 
professionals and among industrial populations or medical 
insurance groups. 

• This Task Group also recommended a mortality data follow-back 
survey to focus on the comparability of the accuracy of cause 
of death, as reported on death certificates and in hospital 
records, for blacks and whites, with particular concern for 
the sensitivity and specificity of coronary heart disease 
ascertainment. The goal would be to determine causes of 
noncomparability and to try to develop programs to reduce the 
oroblems. 



318 



Task Group II focused on the research strategies for ascertaining 
the distribution of known and suspected risk factors for coronary 
heart disease (biochemical and psychosocial) for 
race-sex-socioeconomic status subgroups of the population and their 
relative contribution over time to the development of coronary 
heart disease in these subgroups . 

• They recommended that a large, multicenter, prospective study 
in diverse settings be initiated to determine differences in 
the prevalence of coronary heart disease and associated risk 
factors between blacks and whites. This study would include 
prospective follow-up to determine the relative contribution 
of these risk factors to coronary heart disease events over 
time. Risk factors to be measured would include the standard 
risk factors, health habits, and psychosocial environmental 
factors. Cooperative efforts with the National Center for 
Health Statistics were also recommended. Various instruments 
for measurement of risk factors, especially psychosocial 
variables, would need to be validated in blacks, (This 
recommendation is compatible with the similar recommendation 
from Task Group I.) 

Task Group III focused their attention on possible research efforts 
to determine the effects of various antihypertensive therapies on 
coronary heart disease events in high-risk populations 
(particularly blacks) and to determine whether the metabolic, 
hemodynamic, and side-effects of these treatments are different in 
blacks as compared with whites . 

• The task group recommended a multicenter, randomized, 
double-blind, clinical trial as the best type of study to 
address these issues. Phase I pilot studies, as well as the 
phase II definitive trial, were recommended. The latter would 
be at least five years in duration. 

Task Group IV focused on the issue of obesity as a risk factor for 
coronary heart disease in bl_ack females. 

• They recommended that research is needed to determine the 
relative importance of obesity as a risk factor for coronary 
heart disease in black females. Case-control studies to 
obtain estimates of relative risk were recommended initially 
and then prospective epidemiologic and intervention studies. 

• Methodologic studies to develop tools for assessing coronary 
heart disease risks in blacks compared with whites were also 
recommended. 

• Studies were recommended to assess the value of weight 
reduction on modification of other coronary heart disease risk 
factors in black and white women, stratified by different 
levels of obesity, Methodologic studies may be needed to 
identify effective means for achieving weight loss in 
different subgroups. 



319 



• Research was recommended to determine factors associated with 
and potentially responsible for the observed divergence in 
development of obesity after adolescence in black compared 
with white females. 

Task Group V focused on the problem of apparent greater incidence 
of pre-hospital and sudden death and the lower hospital survival 
rates of blacks following heart attack . 

• This task group recommended survey efforts to learn what level 
of awareness is present among adult blacks regarding risk 
factors and symptoms of coronary heart disease, and to 
investigate and assess the appropriateness of pre-hospital 
behavior by blacks, in response to such symptoms. The goal of 
this research is to obtain information to assist in 
implementing interventions that will reduce mortality and 
morbidity resulting from CHD in black populations. Pilot 
studies and pretests of measurement instruments may be 
necessary. 

• This task group also recommended a study to assess the extent 
of knowledge, attitudes, and practices of health providers in 
diagnosing and treating coronary heart disease in black 
populations. Such a study would also develop appropriate 
educational interventions. 



320 



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Intervention Trial. American Heart J 108(3;2) :839-848, 1984. 

8. Cooper R: Cardiovascular mortality among blacks, hypertension 
control and the Reagan budget. J of the National Medical 
Association 73(11) :1019-1020, 1981. 

9. Cooper R: A note on the biologic concept of race and its 
application in epidemiologic research. American Heart J 108 
(3;2) :715-723, 1984. 

10. Cooper R, Liu K, Stamler J, Schoenberger JA, Shekelle RP, CoUette 
P, Shekelle S: Prevalence of diabetes/hyperqiycemia and associated 
cardiovascular risk factors in blacks and whites: Chicaqo Heart 
Association Detection Project in Industrv. American Heart J 108 
(3;2) :827-833, 1984. 

11. Currv CL, Oliver J, Mumtaz FB: Coronary artery disease in blacks: 
Risk' factors. American^ Heart J 108(3;2) :653-657, 1984. 

12. Davis, Gold, and Makue: Access to health care for the poor: Does 
the gap remain? Annual Review of Public Health 2:159-182, 1981. 

13. Diamond EL: The role of anger and hostility in essential 
hypertension and coronary -heart disease. Psychology Bulletin 92^ 
{21:410-433, 1982. 

14. Francis C, et al.: Summary of Workshop IV: Working group on 
natural history, prevention, and medical and surgical treatment. 
American Heart J 108(3;2) :711-715, 1984. 

15. Garfinkel L: Cigarette smoking and coronary heart disease in 
blacks: Comparison to whites in a prospective study. American 
Heart Journal 108(3;2) :802-807, 1984. 

16. Gartside PS, Khoury P, and Glueck CJ: Determinants of hinh-density 
lipoprotein cholesterol in blacks and whites: The second National 
Health and Nutrition Examination Survey. American Heart J 108 
(3;2) :641-653, 1984. 

17. Gillum RF: Coronary heart disease in black populations. I: 
Mortality and morbidity. American Heart J 104(4;1) :839-851, 1982. 



321 



18. Gillum RF and Grant CT: Coronary heart disease in black 
populations. II: Risk factors. American Heart Journal 104 
(4;l) :852-864, 1982. 

19. Gillum RF and Liu KC: Coronary heart disease mortality in United 
States' blacks, 1940-1978: Trends and unanswered questions. 
American Heart J in8(3;2) :728-73?, 1984. 

20. Gillum RF and Paffenbarger RS: Chronic disease in former college 
students. XVII: Sociocultural mobility as a precursor of coronary 
heart disease and hypertension. American J of Epidemioloqv 
108:289, 1978. 

21. Glueck CJ, Gartside P, Laskarzewski PM, Khoury P, Tyroler HA: 
High-density lipoprotein cholesterol in blacks and whites: 
Potential ramifications for coronary heart disease. American Heart 
J 108(3;2) :815-827, 1984. 

22. Harburg E, Erfurt JC, Chape LS, Hauestein LS, Schull WJ, and Schork 
MA: Socioecological stressor areas and black-white blood pressure: 
Detroit. J of Chronic Diseases 26:595, 1973. 

23. Haywood LJ: Coronary heart disease mortality/morbidity and risk in 
blacks. I: Clinical manifestations and diagnostic criteria: The 
experience with the Beta-blocker Heart Attack Trial. American 
Heart J 108(3;2) :787-794, 1984a. 

24. Haywood LJ: Coronary heart disease mortality/morbidity and risk in 
blacks. II: Access to medical care. American Heart J 108 
(3;2) :794-797, 1984b. 

25. Haywood LJ: Issues in the natural history and treatment of 
coronary heart disease in black populations: Medical management. 
American Heart J 108(3;2) :683-687, 1984c. 

26. Heiss G, Schonfeld G, Johnson JL, Heyden S, Hames CG, Tyroler HA: 
Black-white differences in plasma levels of apolipoproteins: The 
Evans County Heart Study. American Heart J 108(3;2) :807-814, 1984. 

27. House JS: Occupational stress and coronary heart disease: A 
review and theoretical integration. J of Health & Social Behavior 
1^:12, 1974. 

28. Jackson JJ: Urban black Americans. In A. Harwood (Ed.), Ethnicity 
& Medical Care. Cambridge, MA, Harvard University Press, 1981, p 
37. 

29. James SA: Socioeconomic influences on coronary heart disease in 
black populations. American Heart J 108(3;2) :669-672, 1984a. 

30. James SA: Coronary heart disease in black Americans: Suggestions 
for research on psychosocial factors. American Heart J 108 
(3;2) :833-838, 1984b. 

31. James SA, Hartnett SA, and Kalsbeek W: John Henryism and blood 
pressure differences among black men. J of Behavioral Medicine 
6:259, 1983c. 



John Henryism 
The role of 
257, 1984d. 



32. James SA, LaCroix AZ, Kleinbaum DG, and Strogatz DS 
and blood pressure differences among black men. II 
occupational stressors. J of Behavioral Medicine 6 

33. Kasl SV: Social and psychologic factors in the etiology of 
coronary heart disease in black populations: An exploration of 
research needs. American Heart J 108(3;2) :660-669, 1984. 

34. Keil JE, Loadholt CB, Weinrich MC, Sandifer H, and Boyle E: 
Incidence of coronary heart disease in blacks in Charleston, South 
Carolina. American Heart J 108(3;2) :779-786, 1984. 



322 



35. Kleinman JC, Feldman JJ, and Monk MA: The effects of changes in 
smoking habits on coronarv heart disease mortal itv, American J of 
Public^Health 6:795, 1979', 

36. Kobasa, Maddi SR, and Kahn S: Hardiness and health. J of 
Personality and Social Psychology 42:168-177, 1982. 

37. Kuller L, Perper J, and Cooper M: Demographic characteristics and 
trends in atherosclerotic heart disease mortality: Sudden death 
and myocardial infarction. Circulation 52 (Suppl. in) :l> 1975. 

38. Langford HG, Oberman A, Borhani NO, Entwisle G, and Tung B: 
Black-white comparison of indices of coronary heart disease and 
myocardial infarction in the stepped-care cohort of the 
Hypertension Detection and Follow-UD Program. American Heart J 108 
(3;2) :797-801, 1984. 

39. Lasser NL, Grandits G, Caggiula W, Cutler JA, Grimm RH, Kuller LH, 
Sherwin RW, and Stamler J: Effects of antihypertensive therapy on 
plasma lipids and lipoproteins in the Multiple Risk Factor 
Intervention Trial. The American J of Medicine 76 (II-A): 52-66, 
1984. 

40. Leaverton PE, Feinleib M, and Thorn T: Coronary heart disease 
mortality in United States' blacks, 1968-1978: Interstate 
variation. American Heart J 108(3;2) :732-737, 1984. 

41. McDonald R, et al.: Summary of Workshop II: Working group on risk 
factors. American Heart J 108(3;2) :703-706, 1984. 

42. Myers HF: Stress, ethnicity and social class: A model for 
research with black populations. In E.E. Jones and S.J. Korchin 
(Eds.), Minority Mental Health. New York, Praeger Press, 1982, p 
118. 

43. Myers HF, et al , : Summary of Workshop III: Working group on 
socioeconomic and sociocultural influences. American Heart J 108 
(3;2) :706-710, 1984. 

44. Neaton JD, Kuller LH, Wentworth D, and Borhani NO: Total and 
cardiovascular mortality in relation to cigarette smoking, serum 
cholesterol concentration, and diastolic blood pressure among black 
and white males followed up for five vears. American Heart J 108 
(3;2) :759-769, 1984. 

45. Oberman A, and Cutter G: Issues in the natural history and 
treatment of coronary h.eart disease in black populations: Suraical 
treatment. American Heart J 108(3;2) :688-694, 1984. 

46. Rowland ML, and Fulwood R: Coronary heart disease risk factor 
trends in blacks between the first and second National Health and 
Nutrition Examination Surveys, United States, 1971-1980. American 
Heart J 108(3;2) :771-779, 1984. 

47. Savage D, et al . : Summary of Workshop I: Working group on 
epidemiology. American Heart J 108(3;2) :699-703, 1984. 

48. Shapiro S, Weinblatt, Frank CW, and Sager RV: Social factors in 
the prognosis of men following first myocardial infarction. 
Milbank' Memorial Fund Quarterly 48:37-50, 1970. 

49. Sterling R, Graeber GM, Albus RA, Burton NA, Lough FC, and Fleming 
AW: Results of myocardial revascularization in black males. 
American Heart J 108(3;2) :695-699, 1984. 

50. Strong JP, Oalman MC, Newman WP, Tracy RE, Malcom GT, Johnson WD, 
McMahan LH, Rock WA, and Guzman MA: Coronary heart disease in 
young black and white males in New Orleans: Community Pathology 
Study. American Heart J 108(3;2) :747-759, 1984. 



323 



51. The Review Panel on Coronary-Prone Behavior and Coronary Heart 
Disease. Coronary-prone behavior and coronary heart disease: A 
critical review. 'Circulation 63(6) :1199-1215", 1981. 

52. Trevisan M, Ostrow D, Cooper RS, Sempos C, and Stamler J: Sex and 
race differences in sodium-lithium counter-transport and red cell 
sodium concentration. American J of Epidemiology 120(4) :537-541, 
1984. 

53. Tyroler HA: Overview of risk factors for coronary heart disease in 
black populations. American Heart J 108(3;2) :658-660, 1984. 

54. Tyroler HA, Knowles MG, Wing SB, Logue EE, Davis CE, Heiss G, 
Heyden S, Hames CG: Ischemic heart disease risk factors and 
twenty-year mortality in middle-age Evans County black males. 
American Heart J 108(3;2) :738-747, 1984. 

55. Watkins LO: Epidemiology of coronary heart disease in black 
populations: Methodologic proposals. American Heart J 
108(3;2) :635-640, 1984a. 

56. Watkins LO: Coronary heart disease and coronary disease risk 
factors in black populations in underdeveloped countries: The case 
for primordial prevention. American Heart J 108(3;2) :850-862, 
1984b. 

57. Watkins LO: The epidemiology of cardiovascular disease in black 
populations. In R.A. Williams (Ed.), Textbook of Ethnic Medicine. 
New York, McGraw-Hill, in press. 

58. Yelin EH, Kramer IS, and Epstein WV: Is health care use equivalent 
across social groups? A diagnosis-based studv. American J of 
Public Health 73(5) : 563-571, 1983. 



324 



Fig. 1: S.V. Kasi, p. 661 



Socio-envipojmen-.^ , pcychosocial influences 



I. Asyn^ccatic status, risk factor(s) absent 



IS, r 



II. Asymptonatic rtatus, risk factor(sJ present 



III. Subclinical disease susceptible to detection 






IV. Initial tyiiptari experience 



i* 



V. Initial event (diagnostic o^itcria net ) 



I' 



n. Course of disease (repeat episodes, residual disability, etc.) 

Via. Nannl course 

VIb. n<catBent eipericnce 



k 



VII. Msptality (oaae fatality) 



FI9. 1. Developmental schema for coronary heart dis- 
ease: the possible role of race and psychosocial factors. 



325 



Table 2: Keil et al , 1984 



Table II. Incidence* of CHD manifestations by race and sex, 1960-1961 to 1974-1975 







Black males 








Black males 


■, high 


Black fema 


les 


White females 






(N •= 322) 




While 


males (N 


'601) 


SES (S ' 


101) 




(N - 440, 


1 




(N = 71 f 


Manifestation 


n 


Rate 


SE 


n 


Rate 


SE 


n 


Rale 


SE 


n 


Rate 


SE 


n 


Rate SE 


All CHD 


43 


131.7 


18.3 


114 


188.4 


15.5 


4 


61.2 


34.5 


72 


161.0 


17.1 


84 


113.8 11.3 


CHD living 


16 


50.7 


12.6 


60 


95.2 


11.6 


2 


26.0 


26.6 


42 


100.9 


14.8 


50 


67.4 9.2 


AMI 


9 


28.5 


9.9 


51 


80.5 


10.8 


2 


26.4 


26.9 


15 


36.3 


9.4 


27 


36.3 6.9 


Angina pectoris 


7 


22.2 


9.1 


8 


12.8 


4.8 










27 


63.6 


12.1 


22 


29.8 6.4 


CHD death 


27 


79.8 


14.2 


54 


93.8 


11.7 


2 


38.3 


37.4 


30 


62.2 


10.5 


34 


46.3 7.1 


AMI 


12 


35.8 


10.2 


35 


60.5 


9.7 










17 


35.6 


8.4 


18 


24.4 5.5 


Sudden death 


11 


32.2 


9.3 


6 


10.2 


4.6 










6 


13.0 


5.8 


6 


8.2 3.7 


ASHD 


4 


11.7 


7.3 


13 


23.2 


6.4 


2 


44.0 


43.0 


7 


13.8 


5.7 


10 


13.& 4.4 



ASHD ■ Athero«clerotic heart disease. 

'Rates per thousand, age adjusted by indirect method Rates for subheadings not additive. 



326 



FIG. 1: GILLUM & LIU . p. 729 



1000 



SCO 



P 400 



JOG 



200 



100' 



_l I I 1 I 1_ 



_l I I I I I 1_ 




1940 



1950 



1980 



Year 



Fig. 1. Age-adjusted CHD mortality rates per 100,000 
population for U.S. nonwhites aged 34 to 74 years, from 
1940 to 1973. \VM = While males; NM = nonwhite males; 
WF = white females; AT = nonwhite females. 



327 



FIGS. 1 & 2: LEAVERTON, FEINLIEB S THOM. p.p. 733-73^ 



1968-197; 



197J 






1978 



Fig. 1. U.S. age-adjusted CHD mortality for white males 
aged 35 to 74 years. 




y.! 




Fig. 2. U.S. age-adjusted CKD mortality for white 
females aged 35 to 74 years. 



328 



FIGS. 3 S A: LEAVERTON. FEINLIEB S THOH, p.p. IZS'l^f^ 



1968-1372 



1968-1972 





1978 




LOWEST 
NO DATA 




HIGHEST 
SECOND 
THIRD 
LOWEST 
NO DATA 



Fig. 3. U.S. age-adjusted CHD mortality for black males 
aged 35 to 74 years (34 states with data). 



Fig. 4. U.S. age-adjusted CHD mortality for 
females aged 35 to 74 years (34 states with data). 



black 



329 



TABLE i»: TYROLER et. al.. p. 7^1 



Table IV. Multivariate association of risk indicators with time to death (PH) and 20-year cumulative risk of death 
(LRF) m males aged 40 to 64 years (all-cause mortality) in Evans County ^amiuiauve risk ot death 



Blacks 





PH 


LRF 


Intercept 




-5.653 


Age 


0.075' 


0.103* 


SBP 


0.016* 


0.022' 


Cholesterol^ 


-0.020 


-0.041 


Cholesterol'^ 


0.005 


0.010 


Smoking current 


0.547t 


0.49211 


Smoking past 


-0.037 


-0.115 


Quplciet index^ 


-0.480 


0.399 


Queteiet index'^ 


0.053 


-0.081 


Deaths/population 


129/294 




x' 


73 


64 



LSS 



PH 



0.059* 
0.015* 

-0.033 1 
0.009+ 
0.701 + 
0.542!| 

-2.903J 
0.369 J 

68 



Whites 



LRF 



126/276 



4.054 

0.086* 

0.019* 

-0.058 J 
0.015J 
1.071 + 
0.909§ 

-3.513§ 
0.429§ 



55 



•p S 0,001. 

tO.OOl <p £ 0.01. 

JO.Ol < p < 0.05. 

50.05 <p « 0.10. 

D0 10<ps0.20. 

^Significance ba«d on joint contribution. Cholesterol term is calculated as cholesUrolVlOO. 



HSS 



PH 



LRF 



0.059* 
0.012+ 
0.066 1 

-0.0131 
0.862* 
0.347 

-3.676+ 
0.428+ 

48 



88/236 



-6.943 
0.076+ 

0.017+ 
0.0S2} 

-0.0181 
1.195+ 
0.489 

-6.013} 
0.736J 

47 



FIGS. A S 5: TYROLER et. al , p. 7^43 



06 



o 

>- 
Q 

o 



0.5 - 



04 



>:o.3 



CD 

CD 
O 

cc 

^ 0.\ 



WHITE MALES 
BLACK MALES 



130 170 210 250 

CHOLESTEROL 



290 



Fig. 4. Twenty-year risk of dying in relation to cholester- 
ol by race in nonsmoking males aged 40 to 64 years in 1960 
in Evans County. (See Fig. 3 legend for statement on risk 
factor estimates.) 



u.o 


" 






o05 


- 




/ 

/ 


2 






>- 






// 


'-^0.4 


>v 




/--^^-^ 


U- 




^-^ 




o 






•^"'-'•"'''^ •'' 






""^-"^ __ 


■•^■^ . 


^ 03 


^v 


/ 


^ 
** 


_j 




--- -/- " 




CD ^r^ 




/ 




< 0.2 

CD 

o 


- 


y 


WHITE HSS 




/ 


WHITE LSS 


oc 




/ 


BLACK 


^ 0.1 


1 


1 1 1 


I 1 r 1 



130 170 210 

CHOLESTEROL 



250 



290 



Fig. 5. Twenty-year risk of dying in relation to cholester- 
ol by ISS in nonsmoking males aged 40 to 64 years in 1960 
in Evans County. (See Fig. 3 legend for statement on risk 
factor estimates.) 



330 



TABLE 2: TYROLER et. al 



739 



Table II. Risk indicators at baseline (1960) among males 
aged 40 to 64 years ISS in Evans County 





Blacks 


Wh 


ites 




LSS 


HSS 




Mean (±SE) 


Mean (±SE) 


Mean (±SE) 


Age 
SBP 

Cholesterol 
Queteiet index 


50.80 (0.3) 
159.20 (1.8) 
202.70 (2.1) 
3.57 (0.03) 


50.90 (0.4) 
145..50 (1.6) 
207.00 (2.4) 
3.60 (0.03) 


51.10 (0.4) 
140.60 (1.6) 
221.20 (2.5) 
3.69 (0.04) 




Percent 


Percent 


Percent 


Smoking current 
Smoking past 
Smoking ever 


65.5 

5.0 

70.5 


61.9 

8.5 

70.4 


47.2 
11.2 
58.4 



FtG. J:. TYROLER et. al., p. 7^0 




" LOW MID HIGH 40-44 45-49 50-54 55-59 60-64 

TERTILES OF AGE 

SYSTOLIC BLOOD PRESSURE 

Fig. 1. Twenty-year percent mortality (derived from Kaplan-Meier survival curves) by tertiles of SBP 
(age adjusted) and by age in black males aged 40 to 64 years in 1960 in Evans County. 



331 



FIGS. 1 & 2: NEATON et. a1.. p. 763 



60 



• * 

II 



30 



20 



10 



• Black Men 

o write Men 



M«. BlACk M«n: 3.602 
No wrul* Utir 67.4 1B 




I 

<75-«0) 



m 



rv 
(B6-ei) 



Diastolic Btood Pressure Oumttle (rrwn Hg) 



3.724 
6S.242 



3.96S 
61.351 



4.708 
65.051 



V 
<>»i| 



7.491 
66.322 




No B1«CK 

Ho WtMl* 



Hon. 3602 
lil«n. 67.416 



tv 

Diastotic Blood Pressure Ouintile (rrvnHg) 



3.734 
65.242 



3.965 
61.361 



4.700 
65.051 



7.491 
65.322 



Fig. 1. Five-year age-adjusted total mortality rate (per 
1000) by diastolic blood pressure level by race. 



Fig. 2. Five-year age-adjusted CHD mortality rate (per 
1000) by diastolic blood pressure level by race. 



332 



TABLE 1: H. A. TYROLER , p. 659 



Table I. Five-year mortality rates in black and white males by education and presence of LVH at baseline for all 
HDFP stratum I participants and those not receiving medication at baseline: Referred-care males ages 40 to 69 years, 
with entry diastolic blood pressure of 90 to 104 mm Hg* 

% Mortality 



(Deaths) S Crude Age-adjustedi 



LVH-t LVH+ LVH- LVH+ LVH- LVH+ 



All stratum I participants 

WM > HS (18) 446 ( 1) 8 4.0 12.5 

WM = HS (26) 402 ( 2) 10 6.5 20.0 

WM < HS (42) 335 ( 7) 16 12.5 43.8 

BNKHS (56)344 (11)32 16.3 34.4 

Participants not receiving medication at baseline 

WM>HS '(13)347 (1) 8 3.8 12.5 

WM ■= HS (21) 315 ( 0) 7 6.7 0.0 

WM < HS (22) 260 ( 5) 12 8.5 41.7 

BM<HS (41)268 (6)18 15.3 33.3 



4.5 


10.2 


7.0 


21.9 


10.6 


28.6 


15.4 


32.3 


4.4 


10.2 


7.4 


0.0 


7.2 


12.4 


14.9 


33.2 


', editors: 


; Mild hypertension: 



WM ■= While males; BM « black males; HS ■= high school education completed. 

•From Tyroler HA: Race, education, and 5-year moruliiy in HDFP stratum I referred-care males. In Gross F. Stras 

Recent advances. New York. 19S3, Raven Press. , .. ,■ u, j 

tAge-adjusted raies by direct method. Sundard population is age decade distribution of all white males aged 40 to 69 years with eiitrv diastolic blood 

pressure of 90 to 104 mm Hg. 

JLVH determined by ECG. LVH+ defined as major LVH by Minnesou Code; LVH- defined as all uiher;.. 



333 



TABLES 6 S 7 COOPER et. a1 . . o.o . 830-331 



Table Vi. Mean values of cardiovascular risk factors in black and white males and females, by diagnostic category: 
CHA Detection Project* 



Risk factor 


Diagnostic category 


White males 


Black males 


White females 


Black females 


S>-5toIic BP (mm Hg)t 


DM/H 


H4.6 


147.9 


137.0 


146.9 




Non-DM/H 


138.5 


141.8 


131.8 


134.3 


Diastolic BP (mm Hg)t 


DM/H 


84.9 


89.9 


81.1 


88.8 




Non-DM/H 


81.6 


84.6 


77.4 


80.3 


Serum cholesterol (mg/dl) 


DM/H 


210.0 


211.9 


215.3 


209.7 




Non-DM/H 


205.7 


201.9 


208.5 


205.6 


No. of cigarettes smoked/day 


DM/H 


11.6 


10.6 


8.0 


9.2 




Non-DM/H 


9.5 


8.9 


7.1 


5.7 


Relative weight 


DM/H 


1.25 


1.30 


1.20 


1.32 




Non-DM/H 


1.22 


1.22 


1.18 


1.26 



BP = Blood pressure; DM = diabetes mellitus; H 
•Age startdardized. ages 2? to &4 years. 
tExcludes those treated for hypertension. 



hjperglycemia. 



Table VII. All-cause death rates (per ICXK)) in black and 
white males with diabetes or hyperglycemia vs those with 
normoglycemia: CHA Detection Project* 









Black/ 




White 


Black 


white 


Diagnostic group 


males 


males 


ratio 


Diabetes or hyperglycemia 


96.0 (240)t 


95.7 ( 9) 


1.00 


Normoglycemia 


62.3 (618) 


62.7 (45) 


1.20 


Ratio of diabetes and 


1.84 


1.53 




hyperglycemia to 








normoglycemia 









•Age standardized, ages 25 to 64 years. 
INumber of deaths. 



334 



FIGS. 1 - 3: GLUECK et. a1.. p.p. 6l6. 8l8 



•Or 



E 
u 




o- — o While (f . 6-17. n«358 
e — -o While 9 . 6-17. n -326 

• •Black cf . 6-17. n.l 19 

•— •BlacK 9 . 6-17. n- 124 



SO 
TH 



90 95 
TM TH 



Fig. 1. Mean levels of HDL cholesterol (HDLC) in 
healthy, full-term, black and white neonates. (Data from 
Gluecit et al.^') Percentile distribution of HDL cholesterol 
in black and white males and females ages 6 to 17 years: 
The Princeton School District Prevalence Study. (Data 
from Morrison et al.") 



•*r 



•s 



es 



r 




Black 5 . JO-59. n . 13< 
While 2 20-59 n-je3 

?0-55. n-76 
While cf. 20-59, n.306 



»—- « While 5 
■ • Black O" 



_j 



S 10 
TH TH 



25 

TH 



SO 
TH 



75 
TH 



SO 95 
TH TH 



Fig. 2. HDL cholesterol distribution in black and white 
males and females, ages 20 to 59 years: The Cincinnati 
LRC's Princeton School District Prevalence Study. (Data 
from Morrison et al.'') 



100 


- 


il-gO 




U-4 4 




^^^t 




^•se 


H 


■»7 


1 


<.30 


> 


■43 


3 


1I-30 




90 
80 
70 


- 






■ -■; ' 




i 
























60 
SO 


~ 






















. y. 








' ,' 




40 


- 


































30 


- 


































20 


- 


































• 

10 


- 






□E 




mi 




Mi 




lllli'll 








mna 




mil'. 





CHOlDLCI. HDLCt 

f"~~l LDLC1. HDLC* 

fy/^i lDLCl. HDLCI.#8lack« more 

likely lo have 

I I LDLC I. HOLCI predominant 

EZ3 

accounting for 
their hjper 
cho'etterolemia 
than whiles 
lor both 
Children and 
adults. p< .02 



WHITE BLACK 
MALES 
6-19 YRS 



WHITE BLACK 
FEMALES 
6-19 YRS 



WHITE BLACK 

MALES 

20-79 YRS 



WHITE BLACK 

FEMALES 

20-79 YRS 



Fig. 3. Percentage of hjisercholesterolemic subjects (total cholesterol on two consecutive visits > the 
90th percentile) having LDL and/or HDL cholesterol primarily accounting for their hypercholesterolemia. 
These subjects were arbitiarily categorized by having LDL > the agesex-race-specific 95th percentile 
and HDL > the age-sex-race-specific 95lh percentile (at visit 2); LDL > the 95lh percentile and HDL 
<95lh percentile; LDL < the 95th percentile and HDL 2: th.» 95th percentile; and LDL < the 95ih 
percentile and HDL < the 95th percentile. (Data from Morrison et al.-') 



335 



FIG. A: GLUECK et. a1.. p. 819 



Black Excess HDLC, mg/dl 
2 4 6.8 




tMen 



n = 434 
n = 459 
n = 174 
n = 188 



Means covariance adjusted 
for age and education of 
the head of the household 
+, p<.01 



Covariance Adjusted Means 

Ouetelet Calories 

White Black White Black 

1.88 1.93 1939t 1642 

1.90 1.95 2364 2156 

2.39t 2.61 1746* 1464 

2.65 2.72 2520 2450 



tGirls 
E!I^^^^^^^ t Boy s 



Women 



1.88 1.94 1920t 1669 

1.90 1.95 2345 2186 

2.39* 2.61 1746* 1451 

2.65 2.71 2515 2440 



Means covariance adjusted 
for age and occupation of 
the head of the household 
t. p<.01 

Fig. 4. Covariance-adjusted mean levels of HDL cholesterol, Quetelet index, and calories per day in 
randomly recalled, blacks and whites. Means were covariance adjusted, separately for age and education of 
head of household and for age and occupation of head of household. Mean excess of HDL cholesterol 
(blacks above whites) is displayed. (Data from Khoury et al.'-) 



336 



FIGS. 3-5: HEISS et. a1 .. p.p. 809-810 



C -TOTAL (p'.ra) 
C-HDL (pvOOl) 
C-LDL (p«.06) 
C-VLDL (pvoe) 
TG (p«.07) 



-20 -15 -10 



-5 5 

mg/dl 



10 15 20 



Fig. 3. Mean black-white differences in lipids and lipo- 
proteins (males). C = Choksterol; TG = triglycerides. 



H C-TOTAL (pv25) 



C-HDL (p=.l5) 



-1 C-LDL Jtp=.2e) 



C-VLDL (p«.25) 



TG (p= 22) 



-20 -15 -10 



-5 5 

mg/dl 



10 



20 



Fig. 4. Mean black-white difTerences in lipids and lipo- 
proteins (females). C = Cholesterol; TG = triglycerides. 



A-I(p..03) 



*.1](p'.8) 



C-IKp-.OOOl) 



-2 



2 * 6 



10 12 



Fig. 5. Mean black-white differences in HDL apopro- 
teins (males). 



337 



Table 6: L. Garfinkel, p. 803 



Table II. Smoking habits* by sex and race 



Smoking habits 



White male 


White female 


Black male 


Black female 


C-'i) 


(%) 


('■-c) 


(',) 


21.9 


68.5 


23.9 


72.3 


11.4 


0.5 


15.3 


1.5 


17.0 


5,4 


8.2 


3.7 


45.3 


25.1 


47.3 


20.0 


5.0 


6.4 


14.2 


10.9 


8.8 


7.9 


15.4 


5.5 


26.1 


10.0 


16.7 


3.5 


5.4 


0.8 


1.0 


0.1 


4.4 


0.5 


5.3 


2.5 


100.0 


100.0 


100.0 


100.0 



Never smoked 
Pipe or cigar only 
Ex-cigarette 
Current cigarette 

Less than 10 a day 

10-19 a day 

20-39 a day 

40-t- a day 
Other 

Total 



'Percentages have been adjusted for age on the age distribution of the total study population at the start of the study. 



338 



FIGS. 8 & 9: NEATON et. al., p. 767 




2 - 



No. Of Cigartttet Reported (per day) 



■to. aiack tten 11.748 


4.730 


4.905 


1,168 


S39 


■to. WNM M*a 208.481 


21.184 


38.399 


27.044 


30.276 



Fig. 8. Five-year age-adjusled CHD mortality rate (per 
1000) by number of cigarettes reported smoked by race. 



6| 

t • 



>■ c 
o 



. (teck IMn 11.748 
. WM« U*R 208.481 




No of Cigarettes Reported (per day) 



4.730 
21.184 



4.905 
38.399 



1.168 
27.044 



939 
30.276 



Fig. 9. Five-year age-adjusted cerebrovascular disease 
mortality rate (per 1000) by number of cigarettes reported 
smoked by race. 



TABLE 7: NEATON et. al 



768 



Table VI!. Five-year age-adjusted CHD death rates by hypertensive status, cigarette smoking status, and level of 
serum cholesterol for MRFIT black and whit^e males 



Risk factor 



No. of men 



Black 



White 



Age-adjusted rate (5 yr) 



Black 



White 



Black/uhiie ratio 



Diastolic BP <90 mm Hg 










Nonsmoker 










Serum cholesterol <250 mg/dl 


6,094 


127,864 


1.67 


2.40 


Serum cholesterol >250 mg/dl 


1,056 


21,182 


6.86 


6.12 


Smokers 










Scrum cholesterol <250 mg/dl 


6,215 


72,635 


6.21 


5.62 


Serum cholesterol >250 mg/dl 


925 


14,905 


u.os 


10.78 


Diastolic BH >90 mm Hg 










Nonsmoker 










Serum cholesterol <250 mg/dl 


3,669 


46,016 


2.88 


3.86 


Serum cholesterol >250 mg/dl 


929 


13,419 


4.92 


9.88 


Smokers 










Serum cholesterol <250 mg/dl 


3.771 


22,010 


6.42 


11.06 


Serum cholesterol >250 mg/dl 


831 


7,353 


9.04 


17.49 



Total 



23.490 



325.384 



4.83 



6.22 



0.70 
1.12 

1.10 
1.03 



0.75 
0.50 

0.58 
0.52 

0.93 



339 







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c > 

(0 1- 



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(0 



to or 
o 

o 

> 



© 



CO 

o 
o 

SCO 

Kq 

a 
> 
r 




m 



o 

o 
z 
o 
m 



s 
o 
e 
m 



X 

PI 

9 
O 
r 
PI 

O 
^1 
«* 

o 
o 

> 
r 
w 



c 
in 



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z 
o 

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o 

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5 



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B 

o 



C) 



TO 



o 
oo 



340 



TABLES; fe & 7; ROV.'L^ND £ FULWOOD. p.p. 776-777 



Table VI. Mean systolic and diastolic blood pressure and mean serum cholesterol level of adults 25 to 74 years old b> 
race, sex, and survey period, showing standard errors and age-adjusted means: United States, 1971-1975 and 
1976-1980*t 













1971-1975 




1976-1980 






1971 


1975 


1976-1980 




















Age-adjusted 




Age-adjusted 




Risk factor and race-sex group 


Mean 


SE 


Mean 


SE 


meant 


SE 


meant 


SE 


Systolic blood pressure (ram Hg) 


















White males 


132.8 


0.5 


130.5 


0.6 


132.8 


0.5 


130.6 


0.7 


White females 


130.1 


0.5 


125.6 


0.7 


129.4 


0.4 


125,1 


0.7 


Black males 


140.0 


1.6 


133.2 


1.1 


140.4 


1.7 


133.7 


1.1 


Black females 


137.8 


1.4 


130.6 


1.2 


138.6 


1.4 


131.7 


1.1 


Diastolic blood pressure (mm Hg) 


















White males 


83.7 


0.3 


82.3 


0.5 


83.6 


0.3 


82.2 


0.5 


White females 


80.4 


0.4 


78.1 


0.5 


80.1 


0.3 


78.0 


0.5 


Black males 


89.9 


1.0 


85.3 


0.8 


89.8 


1.0 


85.5 


0.8 


Black females 


87.0 


0.9 


82.3 


0.6 


87.1 


0.8 


82.6 


0.6 


Serum cholesterol level (mg/dl) 


















White males 


218.0 


1.1 


216.6 


1.2 


217.5 


1.0 


216.7 


1.1 


White females 


222.8 


1.1 


220.7 


1.2 


221.4 


1.0 


219.9 


1.2 


Black males 


225.5 


4.6 


215.0 


3.3 


225.7 


4.9 


215.4 


3.0 


Black females 


219.4 


2.9 


217.1 


3.2 


221.2 


2.6 


219.2 


2.7 



SE = Standard error of the mean. 

•Data from the National Health and Nutrition Examination Survey. Di\-ision of Health Examination Statistics, National Center for Health Statistics, 

HyatUville. Md. 

tAge adjusted by direct method to the total US population as estimated at the midpoint of the 19761980 N'HANES. 



Table VII. Age-adjusted percent distribution among risk factor groups with standard error of age-adjusted percent for 
selected race-sex groups ages 25 to 74 years by "survey period: United States, 1971-1975 and 1976-1980' 

Risk factor groupst 



None} 



One§ 



Two or more 11 





1971 


1975 


1976-1980 


1971 


-7975 


1976-1980 


1971-1975 


1976- 19S0 


Race-sex group 


% 


SE 


% 


SE 


% 


SE 


% 


SE 


% 


SE 


% 


SE 


White males 


39.0 


1.3 


42.5 


1.1 


46.2 


1.3 


44.5 


1.1 


14.8 


0.8 


13.0 


0.6 


While females 


45.4 


1.1 


47.0 


0.9 


41.9 


1.0 


42.9 


0.8 


12.7 


0.7 


10.1 


0.5 


Black males 


23.4 


3.2 


29.3 


2.0 


44.3 


3.9 


50.9 


2.3 


32.3 


4.1 


19.8 


2.1 


Black females 


28.0 


2.4 


41.4 


2.3 


49.2 


2.5 


43.7 


2.0 


22.8 


1.8 


14.9 


1.2 



SE - Standard error. 

'Data from the National Health and Nutrition Examination Survey, Division of Health Examination Statistics, National Center for Health Statistics, 

HyatUville, Md. 

lAge-adjusted by direct method to the total U.S. population estimated at the midpoint of the 197C 1980 NHAN'ES. 

tNoneof the foliuwing.' lystolic blood pressureof at least IGOmm Hg and/or diastolic blood pressure of at least 95 mm Hg, serum cholesterol level of at least 

260 mg/dl, or smoker. 

{Only one of the above. 

fTwo or more of the above. 



341 



TABLE 5: CONNETT £ STAMLER. o. 8^3 



Tauie V. Mean values at sixth annual visit and percent changes in risk factors from baseline, by study group and 
race 







'si group 






UC group 






White (N 


= 5338) 


Black (N = 


416) 


White (N •= 


5227) 


Black (N = 


411) 




Sixth ann. 




Sixth ann. 




Sixth ann. 




Sixth ann. 




Risk factors 


visit % Change 


visit % 


Change 


visit % 


Change 


visit % 


Change 


DBP (mm Hg) 


80.4 


-11.4 


81.3 


-13.6 


83.5 


-7.9 


85.6 


-8.1 


SBP (mm Hg) 


121.4 


-10.3 


122.3 


-11.7 


126.5 


-6.4 


129.4 


-5.8 


Percent smokers* 


33.3 


-46.2 


38.0 


-43.0 


43.8 


-29.0 


42.9 


-22.5 


Serum cholesterol (mg/dl) 


235.8 


-7.3 


231.0 


-6.0 


240.5 


-5.6 


237.3 


-3.7 


Plasma cholesterol (mg/dl) 


228.5 


-6.4 


224.4 


-6.5 


233.3 


-4.5 


230.2 


-4.3 


Plasma HDL cholesterol (mg/dl) 


41.3 


-2.6 


46.0 


-6.5 


41.4 


-2.6 


47.6 


-4.8 


Plasma LDL cholesterol (mg/dl) 


148.7 


-8.6 


148.3 


-8.5 


152.8 


-6.4 


153.8 


-5.4 


Plasma triglycerides (mg/dl) 


200.9 


+1.7 


153.9 


+7.2 


203.0 


+3.3 


147.1 


+4.0 


Weight (lb) 


187.7 


-0.7 


192.3 


-0.2 


190.1 


+0.7 


190.1 


+0.7 



HDL ■ High-density lipoprotein; LDL ■ low-density lipoprotein. 
'Thiocyanau-adjusted rates, as defined by Neaton et al.' 



342 



Table 5: Langford et a1 , p. 800 



Tabic V. Five-year incidence of angina, ECG MI, history of MI, and MI by RQ for SC participants in HDFP 







Angina 








ECG MI 






Sample size 


Events 


Rate 


So 


mple size 


Events 


Roir 


White males 


1799 


89 


4.9 




1868 


12 


O.fi 


Black males 


983 


54 


5.5 




1056 


15 


1.4 


White females 


1078 


103 


9.6 




1172 


3 


0.3 


Black females 


1211 


79 


6.5 




1329 


10 


0.8 


Total 


5071 


325 


6.4 




5425 


40 


0.8 



343 



Table 1: R. Sterling et a1. p. 696 



Table 1. Operat 


ive mortality (1970-1982) 


Black male patients Other WRAMC patients 


Year 


No. % No. % 


1970-1977* 

1978-1982 

1970-1982 


2/14 14 22/407 5.4 
1/40 2.5 33/916 3.6 
3/54 5.6 55/1323 4.2 



WRAMC • Walter Re«d Amy Medical CcnUr. 
'Prior u> uu of cardioplegia. 



344 



Prevalence and Incidence of 
Ischemic Heart Disease in 
United States' Black and 
White Populations 



Melford J. Henderson, M.A., M.P.H. 

Research Fellow 

Association of Black Cardiologists 

Daniel D. Savage, M.D., Ph.D. 

Medical Advisor 

National Center for Health Statistics 

Hyattsville, Maryland 



A major deficiency of epidemiologic research on ischemic heart disease 
(IHD) in the United States has been the limited amount of reliable 
information published on blacks (1). Published information on the 
prevalence and incidence of IHD in blacks is incomplete and, at least on 
the surface, inconsistent (1). Reliability of data on prevalence of IHD in 
blacks has been compromised by the inclusion of relatively small numbers of 
blacks in population-based studies and/or selection bias in the reported 
study groups. Varying diagnostic criteria and study methods have 
contributed to the apparent confusion. The purpose of this paper is first, 
to review current information on the prevalence and incidence of IHD in 
U.S. black and white populations; second, to document the inadequacy of 
available information; and third, to suggest implications of these data for 
the DHHS Task Force on Black and Minority Health. 

Definition of Ischemic Heart Disease 

Ischemic heart disease in this review includes all of the disorders of 
the heart that result from inadequate supply of oxygen to the myocardium. 
Manifestations are: 

" myocardial infarction (MI), or death of myocardial tissue 
resulting from significant reduction or interruption of 
coronary blood flow; 

* angina pectoris (AP) , a varied symptom complex (most 
commonly including substernal chest discomfort) caused 
by transient ischemia that falls short of producing 
infarction; 

* arteriosclerotic heart disease, defined as obstruction 
of coronary vessels by atherosclerotic plaques leading 
to functional and structural changes in the myocardium 
with or without symptoms ; 

* sudden death, defined as death within seconds to several 
minutes (for some studies, several hours) after the onset of 
symptoms . 

Gillum (2) emphasized that IHD is a major cause of illness in both 
U.S. black and white populations, and is the leading cause of death. 
National data derived from death certificates indicate that it is the cause 
of death in 30-40% of all adult blacks and whites (2). Death from IHD 
occurred at a lower rate in~black men than white men in 1940, increased 
until it exceeded the white death rate in 1968, and then declined to a 
level comparable to that in white men in 1976, but still exceeded the 1940 
rate (2) . Black women appear to have had IHD mortality rates similar to or 
higher than those of white women (2), but comparisons of morbidity and 
mortality are difficult because absolute numbers of cases of IHD in studies 
involving black women are small (2) . 

The 1960-62 National Health Examination Survey (NHES) conducted by the 
National Center for Health Statistics (NCHS) indicated little difference 
between U.S. blacks and whites in prevalence of IHD (3). In a random 
population sample, black and white persons were equally likely to have 
arteriosclerotic heart disease, but the sampling error was too large for 
meaningful, detailed comparison. Electrocardiographic (ECG) data from two 
national probability samples (NHANES 1 and 2) are currently being analyzed 
at NCHS. The data consist of ECGs from nearly 17,000 subjects (age range. 



347 



25-74 years) with a total of about 2000 blacks in the two studies, combined 
(Tables 1 and 2). These data sets are deceptively large. The number of 
black men and women in individual age groups is small, as is the percentage 
with Ml-associated ECG changes. For example, the percent with 
Ml-associated Q-wave Minnesota codes (1-1-1 to 1-1-7) (4) in the white men 
ranged from less than 2% in those age 44-55 years to about 3% in those age 
65-74 years. For black men, the percentages with such codes were similar 
to those of whites in younger men but substantially lower (about 1/2 the 
white male rate) in those over age 65 years. 

In contrast to those for black men, the prevalence estimates for white 
men are relatively stable. For example, the addition of two "cases" in the 
55-64 year age group would double the prevalence of Ml-associated ECG 
findings in black men. The small numbers of blacks in the sample and low 
number of such ECG findings in black and white men in the general 
population do not allow comparisons of prevalence. Differences in ECG 
criteria for Ml-associated changes has added to the confusion in various 
studies. The use of a standardized code (e.g., the Minnesota code) 
contributes to the comparability of various epidemiologic studies. 
However, even this has not resolved all criteria-related issues. For 
example, use of the Minnesota coding system for major Q wave findings 
(e.g., codes 1-1-1 to 1-1-7) allows comparison of these studies with 
others. However, it is possible that this would leave undetected a group 
of individuals who have clinically accepted ECG evidence of MI but do not 
quite meet the criteria for these codes. The addition of other Minnesota 
codes (e.g., 1-2-1 to 1-2-5, 1-2-7, 1-2-8 and various ST and T wave codes) 
increases sensitivity but at the expense of specificity. If these various 
ECG manifestations have the same meaning in blacks and whites, these 
technical considerations would not necessarily invalidate comparisons. 
However, there is some evidence that the meaning of at least some of the 
ECG markers (e.g., some ST-T changes) may be different in blacks and whites 
(4a). 

Some preliminary comparisons can be made between blacks and whites in 
the NHANES studies despite the indicated limitations of the data. The 
prevalence of Ml-associated ECG changes is similar in 45 to 64 year old 
black and white men but greater in older white men than in black men. 
This might be related to the 5 to 7 year shorter life span of black men 
(average life span of about 65 years) such that the group that lives to 65 
includes a larger proportion of those who have not succumbed to IHD at an 
earlier age. Differential case-fatality (discussed below) could also be 
involved. The prevalence of IHD in black women was greater than or equal 
to that of white women (0% in the young to about 1% over age 64) with no 
cross-over . 

The 1972 Health Interview Survey (5) indicated higher age-specific 
self-reported prevalence of heart disease in nonwhites (predominantly 
blacks) than in whites in both age groups 17-44 and 45-64 years. However, 
nonwhites reported the diagnosis of coronary heart disease less often than 
whites in ages 45-64 years (15.5 vs. 36.8 per 1000). 

In some studies, prevalence of IHD was estimated from surveys or 
baseline examinations of population-based cohorts. In 1960, the Evans 
County, Georgia study (6) surveyed nearly all residents in this rural 
county 40-74 years old and 50% of those aged 15-39 years; this resulted in 
3102 participants. Nearly three times as many white men as black men 



348 



reported syndromes of IHD (Table 3A) , with fewer black men reporting IHD at 
all ages. When black and white women were compared, there was no 
significant racial difference in prevalence (14 vs. 18 per 1000). 

In the Charleston, SC study, 2275 blacks and whites were examined in 
1960/61 (7). Age-adjusted IHD rates were computed indirectly using 
standard age-specific rates for the total study sample. In the cohort 
intake of 1960/61, white men of all ages had greater IHD prevalence than 
black men (Table 3B) . Prevalence in black women was identical to that in 
white women (26.6 per 1000). Black women aged 75 years and over had a 
greater IHD prevalence than black men (though not statistically 
significant). Thus, the Charleston and Evans County studies reported 
similar findings on the order of prevalence of IHD (Tables 3A and 3B). 
White men were more likely to have IHD than black men. White and black 
women had almost identical prevalence rates. 

In the Hypertension Detection and Follow-Up Program (HDFP)(8), 
hypertensive participants were evaluated by ECG for evidence of MI and were 
administered the Rose Questionnaire to detect symptoms of AP. AP was found 
to be more prevalent in black men than white men (7.7 vs. 5.1 per 100) and 
more prevalent in black women than white women (9.9 vs. 8.6 per 100). 
Compared to those without AP, those subjects with AP had twice the 
likelihood of death during the ensuing five years. This applied to all 
race-sex groups except black women. 

The prevalence of MI at baseline as determined by the Rose 
Questionnaire was higher in whites (5.9 per 100) than blacks (4.6 per 100), 
and higher in white women (7.2 per 100) than black women (4.2 per 100). 

Incidence of IHD in Black and White Populations 

The study of incidence requires thorough assessment of the population 
at risk, thorough tabulation of cases, and recognition of all indicated age 
and sex differences. Completed population studies yield too few incidence 
cases of acute myocardial infarction (AMI) and do not permit adequate 
assessment of comparative incidence among men and women in black and white 
populations. 

Prior to 1970, studies that compared IHD incidence in blacks and whites 
lacked population-based age-specific data. They usually involved only one 
hospital or group of hospitals. For example, Mihaley and Whiteman (9) 
studied AMI at Harlem Hospital in 1950-54, but during that time only 152 
such cases were admitted. Whites, accounting for 5.8% of admissions, 
constituted 13.1% of infarctions. The investigators maintained that AMI 
was as common in blacks as in whites, but they did not have adequate data 
to support their conclusion. 

Data from NCHS Hospital Discharge Surveys in 1972, 1975, 1978, and 
1981 (10) indicate that men and women over age 45 maintained nearly 
constant hospital discharge rates for AMI. During 1981, rates for black 
men were about 45% of total white rates, while rates for black women were 
about 70% of white rates (ages 45-64). However, these data may be not 
reflect true incidence because they do not take into account subjects who 
died suddenly before hospital admission. 

Few major studies involving the epidemiology of IHD yield data on 
racial incidence. Ongoing prospective studies, such as those conducted in 
Framingham, MA (11) and by the Hospital Insurance Plan of New York (HIP) 



349 



(12), involve predominantly white samples. The HIP study of insured 
persons found the annual age-adjusted rate of incidence of first MI in 
nonwhite (predominantly black) men to be half the rate in white men and the 
case-fatality rate to be higher in nonwhites (47.5%) than in whites 
(35.3%). However, the total number of nonwhite cases was too small to 
yield statistically significant conclusions. 

Additional studies of interest are those carried out in Nashville, TN 
(14); Baltimore, MD (15); Newark, NJ (16); and Columbia (17,17a) and rural 
Pee Dee (17a), SC. These studies reported incidence of hospitalization for 
IHD in blacks and whites by age and sex (Table 7) . 

In the Nashville study (14), 1967-68, hospital surveillance was used 
to detect all cases of AMI and sudden coronary death in persons ages 35-74 
years. Although only 20% of the population group was black, the total 
number of subjects was large (167,000). Annual incidence of MI was 
substantially lower for black men than for white men at each age (Table 4) . 
White men had more than double the rate of black men. Annual incidence of 
AMI was also greater in white women than in black women (Table 4) . In this 
study, black men had greater incidence than black women. In the 1970-72 
Baltimore study (15), the number of nonfatal Q wave ("transmural AMIs") was 
determined from a review of hospital records in the Baltimore area. 
One-third of the 500,000 population sample was black. The incidence of 
"transmural" AMI in white men ages 25-64 years was more than twice the 
incidence in black men; but white women had only slightly greater incidence 
than black women. Black and white women had similar nonfatal MI rates, and 
in Nashville and Baltimore the occurrence of nonfatal MI was twice as 
frequent as sudden death. 

The Newark study (16) involved review of 89.5% of all 1973 hospital 
admissions (15,124) in that city. Age-decade specific MI hospitalization 
rates were reported for seven age groups (Table 5) . When analyzed by 
decade, data revealed no statistically significant difference in incidence 
between white men and black men, but the incidence was slightly higher for 
white men at every decade except 40-49. AMI rates for black women were 
slightly higher than for white women at every decade, but these differences 
were not statistically significant. 

The Columbia, S.C. study (17) in 19 78 examined age-adjusted incidence 
of AMI. The population included patients with prior heart disease and MI, 
as well as those whose sudden death was associated with MI. Both proven 
and suspected MI incidence were included, and in each age group over age 35 
years, white men had higher incidence of Ml than did black men. Black and 
white women under age 65 years showed no consistent difference in 
incidence, but black women ages 66-75 years had somewhat lower incidence. 
Overall frequency was greatest in white men and decreased in the following 
order: black men, white women, black women. 

These studies differ in various ways making a firm conclusion 
regarding the relative incidence of IHD in blacks and whites impossible. 
Inadequacy of the available incidence data is related to several problems 
including: 

" the limited number of studies that have been carried out; 

" the inadequate numbers of blacks in the populations studied; 

" the use of varying standards for age-adjustment; 

" the use of varying diagnostic criteria; 

" varying lengths of follow-up. 



350 



Data from the Newark and Baltimore studies indicate little difference 
in incidence between white and black women. These population studies found 
a greater incidence of AMI in white men than in black men. However, 
observations from elsewhere on patterns of access to hospital care suggest 
that the lower number of hospital admissions among black men may have been 
due to a greater frequency of out-of -hospital deaths. Another factor may 
have been the difficulty in diagnosing AMI in blacks due to a greater 
incidence of MI without diagnostic Q waves, so-called "nontransmural" MI. 
Comparison of black and white subjects enrolled in the Beta Blocker Heart 
Attack Trial after MI suggests that blacks are somewhat less likely to 
manifest Q waves than whites (24). The Nashville and Baltimore studies 
excluded cases of non-Q wave MI, but the Newark study defined "transmural" 
as well as "nontransmural" MI. The ECG is known to be inadequate in making 
this distinction. 

While the Newark and Nashville studies used ECG, autopsy, and enzyme 
data as criteria for diagnosing AMI, the Columbia study used those criteria 
only to find definite MI; they employed another category, "possible Ml" 
(i.e., MI which was suggested by medical histories). This may contribute 
to the variation in their findings regarding AMI in black vs. white women 
under age 65 . 

Incidence of IHD in Cohort Studies 

Two cohort studies assessed incidence of IHD in blacks as well as 
whites. In the Charleston study (7), 2275 blacks and whites of both sexes 
were enrolled in 1960-62 and the incidence of CHD was assessed in the 
ensuing 14-year period (1974-75). White men and black women were found to 
have the highest incidence (Table 6) . Incidence for white men exceeded 
that for black men. One hundred and one black males were also selected on 
the basis of high socioeconomic status (SES) . Their AMI and IHD rates were 
shown to be half those of the community sample of black males. Black women 
showed a higher incidence of AP than all other groups. White men had the 
highest incidence of both fatal and nonfatal AMI . 

The Evans County study (13) involved assessment and followup of a 
relatively small cohort of black men and women and a much larger cohort of 
white men and women. This biracial sample of 3102 persons was initially 
examined between 1960 and 1962. From this original cohort, 2530 persons 
were reexamined between 1967" and 1969 and incidence rates of IHD for the 87 
month period were determined. The study indicated a higher age-adjusted 
incidence of AMI by ECG or autopsy in white than in black men (33.6 per 
1000 vs. 11.4 per 1000). Significant differences were not found between 
white and black women but the absolute numbers of cases were small. 

Some differences in reported incidence are seen in the Charleston (7) 
and Evans County studies (13). For example, in Evans County, black men and 
women had lower incidence of IHD than white men and women; in Charleston, 
their rates of incidence were comparable to the incidence of IHD in whites. 
In the Charleston study, black women had the highest incidence of AP, 
double the rate in white women, triple the rate in black men, and almost 
five times the rate in white men. (The HDFP data, cited earlier, suggest 
that positive responses to Rose Questionnaire for AP may have different 
pathophysiologic significance in black women than in other race-sex 
groups). In contrast, results from the Evans County study showed that AP 



351 



rates in black men were almost double that of white men, however the number 
of cases for women were too small for meaningful comparisons. The time of 
observation was 162 months for the Charleston study, and 87 months for the 
Evans County study. Incident cases of MI were identified by ECG in the 
Evans County study, and the Charleston study determined incident cases of 
MI and AP by means of the Rose Questionnaire, a technique that has not been 
adequately validated in blacks. This questionnaire is more likely to yield 
overestimates of disease frequency than conservative ECG estimates. 

In-hospital vs. Out-of-hospital Mortality Rates 

In incidence studies, mortality estimates have been obtained largely 
by comparing patients who were treated for AMI in hospitals. The Baltimore 
study (15) found that black men had twice as many sudden deaths as nonfatal 
MI and were discharged alive from the hospital less often than white men. 
This finding suggests relatively high prehospital death rates and 
case-fatality among black men. 

A review of death certificate data from the Newark surveillance study 
found 517 individuals declared "dead on arrival" (DOA) in whom the death 
could be attributed to IHD (16). Analysis by race, sex, and age decade 
(ages 20-80) showed that the frequency of DOA among blacks was strikingly 
higher than among whites in almost every age group except for men over age 
70 years. Under age 70 years, the incidence was higher for black men than 
black women, but over age 80 black women had a much higher rate. The total 
hospital mortality from AMI was higher for black men than white men (32% 
vs. 22%), but white women had twice the mortality of black women (40% vs. 
16%). Q wave ("transmural") and non Q wave ("non transmural") infarcts 
detected by ECG were found in equal numbers in black men and black women. 

After exclusion of diagnosed cases of MI, subjects declared DOA 
comprised 52% of sudden death in the Nashville study (14). More of the 
whites (55%) than blacks (45%) were DOA (p<0.05), but no stratification by 
age was reported. White men were more apt than black men to respond to 
symptoms of impending MI by seeking medical care, and more white than black 
women saw a physician prior to death. These apparent differences in health 
knowledge, attitudes, and behavior may account for racial differences in 
disease outcome. 

The Nashville and Newark studies differed markedly in many ways. The 
Newark sample was almost eight times as large as that of Nashville, and was 
55% black compared to 20% in Nashville. Although both groups of 
investigators evaluated DOA by death certificate and defined sudden death 
as death occurring within 24 hours of onset of symptoms, the Newark group 
included sudden deaths from unknown causes as well as deaths attributable 
to arteriosclerotic heart disease, while the Nashville group used the 
clinical criteria established in the HIP study (12) for an overwhelmingly 
white population. The Newark group excluded death due to trauma, cancer, 
or other identifiable cause; the Nashville study excluded persons over 74 
years, persons restricted to home, hospital, or other institutions. 

The two groups also used different criteria to diagnose AMI. The 
Nashville group used one or more of the following: autopsy, clinical 
examination, or ECG. In the Newark study, both "transmural" and 
"nontransmural" MI were diagnosed. Despite these differences, the data 



352 



from the studies do suggest that the lower number of hospital admissions of 
black men for AMI may at least partially, be explained by the greater 
number of out-of -hospital deaths. 

Incidence of Sudden Death 

Sudden death comprises a large segment of total IHD death in U.S. 
black and white populations; however, as with other IHD end points, few 
reliable population-based data are available with regard to blacks. It is 
generally acknowledged that sudden death results from some type of 
arrhythmia- -either asystole or ventricular f ibrillation--and may have 
different underlying pathophysiological mechanisms from those of 
demonstrable AMI. The Charleston study (7) revealed sudden death in black 
men (32.2 per 1000) to be three times the rate in white men (10.2 per 
1000). The rate in black women (13 per 1000), was 1.5 times the rate in 
white women (8.2 per 1000). 

In the 1967-68 Nashville study (14), investigators identified likely 
cases of sudden death from death certificates of people aged 35-74 years 
and then interviewed relatives or friends to confirm the diagnoses. The 
study showed black men to be at slightly greater risk of dying suddenly 
from apparent IHD than white men. The death rate was greater in black men 
(2.80 vs. 2.20 per 1000) than in white men. Black women had greater rates 
than white women (1.48 vs. 0.70 per 1000). 

The Baltimore study (15) measured total IHD rate and sudden death 
rate. Sudden death rates were similar for black and white women. The rate 
for black men was somewhat higher than for white men. No significant 
racial differences were found in the incidence of sudden death, with or 
without prior history of heart disease, but the number of sudden deaths was 
very small for black women. The incidence of instantaneous death (defined 
as death within 15 minutes of onset) was the same in black and white women, 
but was slightly lower in black men than in white men. 

In the Nashville study, more sudden deaths occurred within two hours 
of symptom onset than in the Baltimore study, but fewer unwitnessed deaths 
were recorded. Ratios of sudden death between white men and women were 5:1 
for Baltimore and 3:1 for Nashville. Male-to-female ratios in blacks were 
identical (2:1) in both studies. 

The variation in statistics on incidence of sudden death may be 
traceable at least partially to the following: 

* varying definitions of terms, 

" varying population samples, and 

" inaccurate death certificates. 
The Charleston study defined sudden death as death within one hour. 
The Baltimore and Nashville studies defined it as death within 24 hours of 
symptom onset. The HIP study (12) defined sudden death as death occurring 
within 48 hours of symptom onset. Such conflicts in definition limit 
possible inferences from the studies. 

Population samples, too, varied from study to study. Baltimore studied 
a slightly younger population than Nashville, and the HIP study included 
only first MI, while the Nashville study included subsequent Mis. In 
addition, the HIP cohort consisted mostly of employed (and therefore 
relatively healthy) individuals, in contrast to the free-living population 



353 



in the Nashville study. These variations may account for the rate of 
sudden death in Nashville being higher for all age groups than in the HIP 
study. 

Inaccuracy of death certificates may also be a significant problem in 
available data. This is suggested by the comparison of the Baltimore study 
results with the 1975 findings of Kuller et . al. who reviewed government 
vital statistics published for Baltimore (18). Nonwhite death rates from 
IHD were found to be higher here than those reported in the 1970-72 
Baltimore study, with a higher sudden death rate for black women than white 
women; little racial difference was found among men. In a representative 
sample, death certificate diagnosis of IHD was confirmed by other data for 
only 67% of black men and 52% of black women. The black male-female rate 
ratios was higher in the Baltimore study than in the official vital 
statistics, suggesting that vital statistics may not be a valid source of 
information on IHD trends in urban black populations. Since death 
certificates were also a primary source in the Nashville study, these 
findings call into question its conclusions. 

Incidence of IHD as Determined by Post-mortem Examination 

Another method for assessing the incidence of death from IHD is 
postmortem examination, particularly those in which autopsied cases are 
representative of either all deaths or a definable sample of deaths. 
Investigators in the Baltimore study performed detailed autopsies of 87% of 
all sudden deaths occurring in a section of Baltimore and certified by the 
medical examiner (15,18). In a total of 169 sudden deaths, 58% of black 
men and women had severe three or four-vessel coronary artery stenoses, 
compared with 70% of white men and 34% of white women (18). In the 118 
cases without prior history of coronary heart disease, black men had acute 
coronary thrombi less frequently than white men (16% vs. 26%). However, 
black and white men had approximately the same frequency of hemorrhage and 
plaque. As noted by Gillum (2) these investigators found greater heart 
weights in blacks, but they found fewer recent (6% vs. 13%) and old (26% 
vs. 43%) myocardial infarctions in black men. 

Assessment of Trends in Morbidity and Mortality in Blacks and Whites 

Moriyama et. al. (19) and Cooper (20) have summarized cardiovascular 
mortality in the U.S. in the last four decades. Gillum (2) points out that 
prior to the 1940s, mortality trends were difficult to assess due to 
inadequacies in reporting, diagnosis, and certification. Data from 
national statistics have consistently shown rates for white men to exceed 
those of nonwhite men, while rates for nonwhite women have exceeded those 
of white women since 1950 (21). It should be noted that in these early 
data, national statistics compared whites and nonwhites , with no direct 
comparison between whites and blacks (who comprise 85% of U.S. nonwhites) 
(19). 

The data show that mortality due to IHD seems to be greater in urban 
than suburban areas, but that mortality has declined nationwide (2,20). 
The only exceptions are the Pacific and Mountain states, where the number 
of deaths attributed to IHD increased in nonwhites aged 35-74 years in both 



354 



sexes between 1940 and 1960 (2). Gillum (2) discussed the rate of decline 
from region to region, finding it greatest in the Northeast and least in 
the Southwest. 

A 1969-77 study in South Carolina (22) showed consistently higher IHD 
mortality rates for blacks compared to whites. Two selected areas were 
surveyed, metropolitan Columbia and rural Pee Dee. [Pee Dee is thought to 
have the highest cardiovascular disease mortality in the South and possibly 
the nation (22)]. Declines in mortality were observed for both blacks and 
whites . 

Conclusions and Implications 

The most evident implication of this review is that prevalence and 
incidence data on IHD in blacks are inadequate, confusing, and must be 
improved. Studies to obtain these data should be population-based and 
should include adequate numbers of subjects. A sufficient number of blacks 
should be included in cohort studies to determine incidence rates of IHD by 
age and sex. Well -validated, consistent criteria should be used. The 
available data suggest an excess prevalence of IHD in black women compared 
to white women, with appreciable absolute rates only after age 64. In 
contrast, white men have a substantial excess prevalence of IHD compared to 
black men after age 64 years. Preliminary HANES data suggest that at 
younger ages, black men have greater or equal prevalence rates of IHD than 
white men but at older ages, as noted, the rate in white men exceeds that 
in black men. If this is substantiated, it could explain some of the 
apparent conflicts in available data. It also underscores the importance 
of having samples of adequate size to allow the use of age-specific 
analyses. Finally, most of the epidemiologic studies reviewed above have 
focused on the supply aspects of IHD (i.e., obstructive coronary disease). 
The autopsy data (15,18) and recent echo data (23) suggest that 
substantially more attention needs to be given to the demand side (i.e., 
left ventricular hypertrophy) as a potential major contributor to the 
morbidity-mortality gap between blacks and whites. 

Acknowledgements 

We gratefully acknowledge the careful reading of the manuscript and 
helpful suggestions by Richard Gillum, M.D., Lucile Adams, Ph.D., Judi 
Kesselman-Turkel, Jaqueline P. Davis, and Sandra J. Anderson. We also 
thank Wilbur Hadden for analytical help with the HANES ECG data, Carla 
Weinberg for technical assistance, and Jackie Adams for secretarial 
support. 



355 



Table 1 

TOTAL NUMBER OF SUBJECTS WITH EGG READINGS 

IN THE NATIONAL HEALTH AND NUTRITION 
SURVEY 1971 - 1975 (PreIiminary-1/28/85) 









Age Group 








ALL 


25-44 


45-54 


55-64 


65-74 


Black men 


379 


120 


97 


75 


87 


White men 


2688 


1037 


636 


528 


487 


Black women 


465 


191 


105 


84 


85 


White women 


3152 


1329 


739 


556 


528 



Table 2 

TOTAL NUMBER OF SUBJECTS WITH EGG READINGS 

IN THE NATIONAL HEALTH AND NUTRITION 
SURVEY 1976 - 1980 (Preliminary-1/28/85) 









Age Group 








ALL 


25-44 


45-54 


55-64 


65-74 


Black men 


528 


209 


62 


129 


128 


White men 


4302 


1554 


617 


1086 


1045 


Black women 


635 


248 


100 


135 


152 


White women 


4794 


1726 


647 


1176 


1245 



356 



Table 3A 

PREVALENCE OF CORONARY HEART DISEASE IN BLACKS AND WHITES AGE 15-75+ 
YEARS PER ONE THOUSAND SUBJECTS, (1960) EVANS COUNTY, GA 

N n Rates* 



Black men 


537 


12 


White men 


947 


54 


Black women 


646 


9 


White women 


972 


18 



22, 


.4 


59, 


.0 


13, 


,6 


18, 


.2 



N= number of persons in each race/sex group 
n=number of cases 

* Age-adjusted rates by indirect method using total population 
as standard 

Source: JC Cornoni et al, Ref 6a 



Table 3B 

PREVALENCE OF CORONARY HEART DISEASE IN BLACKS AND WHITES AGE 35-75+ 
YEARS PER ONE THOUSAND SUBJECTS, (1960-61) CHARLESTON, SC 

N n Rates* 



Black 


men 


333 


11 


White 


men 


650 


49 


Black 


women 


453 


13 


White 


women 


738 


20 



32, 


,7 


75, 


.8 


26, 


,6 


26, 


.6 



* Age adjusted by indirect method 
Source: Keil JE et al, Ref 7 



357 



Table 4 

INCIDENCE OF ANTERIOR MYOCARDIAL INFARCTION IN BLACKS AND WHITES AGE 
35-74 YEARS PER ONE THOUSAND SUBJECTS, (1967-68) NASHVILLE, TN 

N n Rates* 









*■ ~ " 


Black 


men 


14,628 


31 


White 


men 


64,478 


379 


Black 


women 


16,236 


18 


White 


women 


71,469 


137 



2.12 
5.88 
1.11 
1.92 



N= number of persons in each race/sex group 

n= number of cases of AMI 

" Age group specific data showed similar trends 

Source: Hagstrom RH et al, Ref 14 



Table 5 

INCIDENCE OF ACUTE MYOCARDIAL INFARCTION IN BLACKS AND WHITES 
PER ONE THOUSAND SUBJECTS BY AGE DECADE, (1973) NEWARK, NJ 



Age Decade Total Cases 



20-29 30-39 40-49 50-59 60-69 70-79 80+ 



Black men 


- 


- 


1.16 


2.41 


4.61 


4.04 


2.27 




- 


- 


(11) 


(15) 


(17) 


(6) 


(1) 


White men 


0.10 


0.78 


1.09 


3.38 


5.37 


6.28 


2.41 




(1) 


(7) 


(11) 


(34) 


(41) 


(27) 


(4) 


Black women 


0.10 


0.19 


0.85 


1.64 


2.18 


4.04 


5.58 




(2) 


(3) 


(4) 


(12) 


(10) 


(8) 


(4) 


White women 





0.11 


0.28 


0.88 


1.31 


3.43 


3.28 




- 


(1) 


(3) 


(10) 


(12) 


(21) 


(8) 



50 



125 



43 



55 



Numbers in parentheses represent numbers of cases 
Source: AB Weisse et al, Ref 16 



358 



Table 6 

INCIDENCE OF IHD MANIFESTATIONS BY RACE AND SEX, 1960-1961 
TO 1974-1975, CHARLESTON, SC 



Black men 
(N=322) 



White men 
(N=601) 



Black men, high SES 
(N=101) 



Manifestation 



n 



Rate 



n 



Rate 



All IHD 


43 




131.7 


All nonfatal IHD 


16 




50.7 


AMI 


9 




28.5 


Angina pectoris 


7 




22.2 




Black 


women 




(N= 


=440) 


Manifestation 


n 




Rate 


All IHD 


72 




161.0 


All nonfatal IHD 


42 




100.9 


AMI 


15 




36.3 


Angina pectoris 


27 




63.6 



,__ 




.14 


188.4 


60 


95.2 


51 


80.5 


8 


12.8 


Whit 


e women 


(N= 


718) 


n 


Rate 


84 


113.8 


50 


67.4 


27 


36.3 


22 


29.8 



4 
2 
2 




Rate 



61.2 
26.0 
26.4 




N= Total number of persons in each race/sex group 

n= Total number of cases in each IHD category 

SES=socioeconomic status 

* Rates per one thousand, age adjusted by indirect method 

Source: JE Keil et al, Ref 7 



359 



Table 7 

INCIDENCE OF HOSPITALIZATION RATES FOR AMI IN U.S . BLACK AND WHITE 
POPULATIONS PER ONE THOUSAND SUBJECTS 



Age/ Sex Evans County, GA 


Nashville 


Baltimore 


Newark C< 


Dlumbia,SC 




1960-1967 


1967-1968 


1970-1972 


1973 


1968 


35-44 














Black 


men 


1.79 


1.02 




- 


0.84 


White 


men 


8.28 


1.84 




0.783 


1.25 


Black 


women 


3.72 


0.19 




0.193 


0.38 


White 


women 


0.69 


0.20 




0.113 


0.06 


45-54 














Black 


men 


5.79 


1.55 


0.6 


1.16 


3.97 


White 


men 


10.48 


5.50 


1.9 


1.09 


5.76 


Black 


women 


5.10 


1.41 


0.2 


0.85 


0.68 


White 


women 


4.14 


1.05 


0.4 


0.28 


1.33 


55-64 














Black 


men 


1.52 


3.47 


0.8 


2.41 


7.61 


White 


men 


17.79 


9.82 


2.9 


3.38 


10.75 


Black 


women 


8.97 


1.64 


1.0 


1.64 


2.91 


White 


women 


5.52 


2.77 


1.1 


0.88 


2.56 


65-74 














Black 


men 


8.69 


3.87 




4.61 


6.27 


White 


men 


32.14 


12.75 




5.37 


18.82 


Black 


women 


6.21 


1.77 




2.18 


5.75 


White 


women 


19.72 


6.49 




1.31 


8.47 



Source: RF Gillum, Ref 2 



360 



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Press, p. 49. 

20. Cooper R, Stamler J, Dyer A, Garside D: The decline in 
mortality from coronary heart disease, U.S.A., 1968-1975. 
J Chronic Disease 1978;31:709. 



362 



21. Rosenberg, HM and Klebb, AJ: Trends in cardiovascular mortality 
with a focus on ischemic heart disease: US, 1950-76 in 
Proceedings of the Conference on the Decline in Coronary Heart 
Disease Mortality. U.S. DHEW, Public Health Services, NIH 

Pub. No. 79-1610, May 1979. 

22. Keil JE, Lackland DT, Hudson MB, Saunders DE Jr, et al: 
Coronary heart disease and stroke mortality in South Carolina 
geographical and temporal trends. J SC Med Assn 1983; 

79:65. 

23. Savage DD: Echocardiographic assessment of cardiac anatomy 
and function in black and white hypertensive subjects. In 
Williams R, ed. Textbook of Ethnic Medicine (in press). 

24. Haywood LJ: Coronary heart disease mortality/morbidity 
and risk in blacks. Clinical manifestations and diagnostic 
criteria: The experience with the Beta BLocker Heart Attack 
Trial. Am Heart Journal 1984; 108 : 787 . 

Supplemental References 

Ahmed SS, Razefort R, Franciato R: Incidence of acute 
myocardial infarction among blacks in an urban community. 
J Med Soc NJ 1977 ;74: 1058. 

Five-year findings of the hypertension detection and follow 
up-program II. Mortality by race, sex and age. JAMA 1979; 
242:2572. 

Kleinbaum DG, Kupper LL, Cassel JC, Tyroler NA: Multivariable 
analysis of risk of coronary heart disease in Evans County, 
Georgia. Arch Intern Med 1971;28:943. 

Kleinman JC, DeGruttola VG, Cohen BB, Madans JH: Regional 
and urban-suburban differentials in coronary heart disease 
mortality and risk factor prevalence. J Chronic Dis 1981; 34: 11. 

Kuller L: Sudden and unexpected nontraumatic deaths in adults. 
A review of epidemiological and clinical studies. Journal of 
Chronic Diseases 1966; 19 : 11652. 

National Center for Health Statistics: Mortality, United States, 
1977. By Number of Deaths. Washington, D.C., 1981, U.S. 
Government Printing Office. 

Stamler J, Berkson DM, Lindberg HA, Miller OW, Hall Y: Racial 
patterns of coronary heart disease: blood pressure, body weight, 
and serum cholesterol in whites and negroes. Geriatrics 
1961;16:382. 



363 



Differences in 
Socioeconomic Status and 
Acculturation among 
Mexican Americans and 
Risk of Cardiovascular 
Disease 




Helen P. Hazuda, Ph.D. 

Division of Clinical Epidemiology 

Department of Medicine 

University of Texas Health Science Center at San Antonio 

San Antonio, Texas 



Introduction 

The pixrpose of this paper is to review the available literature 
to assess the extent to vAiich increasing differences in socioeco- 
ncxnic status (SES) and acculturation among Mexican Americans are 
associated with differences in cardiovascular risk factors and to 
make public health reconmendations based on the findings. It^ 
should be noted initially that there is no oocnmonly agreed upon 
definition of Mexican American (MA) ethnicity and that the 
several indicators most comnnonly used to classify persons as 
Mexican American identify populations v^ich differ significantly 
in corposition and size (1-5). The studies reviewed in this 
paper relied on a variety of indicators for Mexican American eth- 
nicity, ranging fron simple self -definition to a complex 
algorithm v^ich considers surname and birthplace of subject's 
parents, ethnic origin of subject's grandparents, and subject's 
preferred ethnic identity. The study populations were referred 
to variously as Hispanics, Spanish- Americans, persons of Spanish- 
surname, Mexican Americans, or ^fexican origin Hispanics. I have, 
nonetheless, restricted this review to studies vi^ich explicitly 
identified the target population as ^texican origin Hispanics or 
were carried out in a geographic region vrfiere the overwhelming 
majority of Hispanics are known to be Mexican origin, (e.g., over 
80% of Hispanics in California and over 92% in Texas are Mexican 
origin (6)). To place the review in context I will begin by pre- 
senting a brief overview of ciianges in socioeconomic status and 
acculturation vAiich have occurred among Mexican Americans during 
the last several decades, and, then, document the role of car- 
diovascular disease as a cause of nortality in this ethnic group 
before moving to a review of cardiovascular risk factors. 

Socioecononic Status and Acculturation of Mexican Anericansl 

The three major indicators of socioeconcxnic status are education, 
occupation, and income. Of these, education is perhaps the most 
important since it is closely linked to upward mobility and the 
acculturation process. At the time of the 1970 census, Mexican 
Americans still lagged about a generation behind the total U.S. 
population in educational attainment and, together with the 
Puerto Ricans, ranked as the least schooled Hispanic subgroup. 
Nevertheless, Mexican Americans had made substantial gains in 
schooling over the last several decades. Around the time of 
World War I only about 10 percent of high-school-ooopletion age 



Statistics reported in this section, unless otherwise indicated, 
were abstracted fron Reference 7: Jaffe AJ, Cullen RM, Boswell 
TD: The Qianging Datiography of Spanish Americans. New York: 
Acadonic Press, 1980. 



367 



Mexican Americans had actually completed high schcxDl. By the end 
of World War II about 20 percent were high school graduates and, 
by 1970, over 50 percent of the school -age cohort of U.S. -born 
Mexican Americans and 32 percent of the Mexico-born cohort were 
high school graduates. Gains were made in higher education as 
well, but in 1970 only about 4 percent of Mexican Americans aged 
25-29 who entered college had actually completed a 4-year degree. 
Occupations held by Mexican American men in 1970 were the lowest 
among the Hispanic subgroups and fell substantially below those 
of non-Hispanic Whites . Nonetheless , considerable i:ptfard move- 
ment occurred among Mexican Americans during the past several 
decades. In fact, the movement of Mexican Americans up the occu- 
pational ladder between 1930 and 1970 was relatively greater than 
that for the total U.S. White male population. A major reason 
for this was the novement of Mexican American men out of agri- 
culture. In 1970 only 10 percent of Mexican American men were 
onployed in agriculture compared to 40 percent in 1930. In addi- 
tion, in 1970 less than 25 percent of Mexican American men were 
on the bottom rungs of the occupational ladder (nonfarm and farm 
laborers) compared to 66 percent in 1930. While 61 percent of 
Mexican American men in 1970 were anployed in lower level blue 
collar jobs ccxipared to only 45 percent of non-Hispanic Whites, 
this figure represented a substantial decline frcm 1930, v*ien 87 
percent of Mexican American men were employed in such jobs. In 
addition, the number of Mexican American men employed in v^ite 
collar jobs at both ujper levels (professionals, nonfarm mana- 
gers) and lower levels (sales and clerical workers) tripled bet- 
ween 1930 and 1970. Within equal levels of schooling the 
occupational positions of Mexican American men closely approached 
those of non-Hispanic Whites; among college graduates, there were 
few differences between the two ethnic groups. 

Overall, about 37 percent of Mexican American women aged 16 and 
over were in the labor force in 1970, ccampared to 41 percent of 
non-Hispanic White wcmen. The occupational position held by 
Mexican American women in 1970 were the lowest for all the 
Hispanic subgroups and fell substantially below those of 
non-Hispanic Whites. Between 1950 and 1970, however, Mexican 
American wonen had experienced considerable upward occupational 
mobility comparable to that for Mexican American men. The number 
of Mexican American women in upper level white collar jobs 
increased from 7 percent in 1950 to 8.5 percent in 1970. In 
lower level white collar occupations, the number of Mexican 
American women increased from 21 percent in 1950 to 31 percent in 
1970. At comparable levels of schooling, Mexican American women 
closely approximated the occupational levels achieved by 
non-Hispanic Whites. 



368 



The income of Mexican Americans still lags substantially behind 
that of non-Hispanic Whites. In 1969 the iredian family incane of 
Mexican Mericans was $6,960, ranging from a median of $1,800 in 
families with no earners to a median of $9,080 in familes with 
two or more earners. These figures compared to a median family 
income among non-Hispanic Whites of $10,100, ranging frcm a 
median of $2,970 in familes with no earners to a median of 
$12,350 in familes with two or more earners. In general, fami 
lies headed by men had higher median inccxnes than families headed 
by wcxnen, and families headed by U.S. born MAs had higher incomes 
than families headed by Mexican born MAs. There is sane indica- 
tion, however, that MAs are gaining ground on non-Hispanic 
Whites. In 1969, MA families headed by males averaged about 65% 
of the incane of non-Hispanic White male-headed families. By 
1976-1978, this percentage had increased to about 70 percent (MA 
median incane, $12,600). Similarly, in 1969 MA families headed 
by f onales averaged about 50 percent of the income of 
non-Hispanic White fonale-headed families. Ey 1976-1978, this 
percentage had also increased to about 70 percent (MA median 
income, $6,200). 

Acculturation can be understood as a canplex process vAiereby 
individuals v^ose primary learning has been in one culture take 
over characteristic ways of living from another culture (8-10). 
This process is canplex in that it usually proceeds some^A^at un- 
evenly in two najor areas of life: the social and the cultural. 
The social area involves interaction with manbers of the host 
society v^ich results in the adoption of the public behaviors, 
language, and material culture of the host society, while pre- 
serving the primary attitudes, values, language and behaviors of 
the culture of origin for participation in the private spheres of 
life. The cultural area involves psychological integration with 
the host society which results in the adoption of the central 
attitudes and values of the host society for participation in 
both public and private spheres of life. On a national level, 
two statistical measures can be examined as indicators of 
acculturation among Mexican -Americans: the proportion who are 
first, second and third generation Americans; and the proportion 
v^o marry outside their own ethnic group (outmarriage), par- 
ticularly those who marry non-Hispanic Whites. 

In 1910 about 58 percent of all MAs in the U.S. were first 
generation Americans (born in Mexico); by 1970 that number had 
dropped to about 32 percent (7). In the five Southwestern states, 
2 \n^ich contain about 90 percent of the total Mexican American 



2 
California, Texas, (Colorado, New Mexico and Arizona. 



369 



popiolation, only 12 percent of MAs were first generation 
Americans in 1970 (11). Another 30 percent were second genera- 
tion (U.S. born of Mexico-born parents), vAiile 58 percent, the 
vast majority, were third generation Americans (U.S. -born of 
U.S. -born parents) (11). 

The rate of outmarriage among U.S. -born MA wcmen in 1970 was the 
lowest among U.S. -born Hispanic wonen.-^ Only 16 percent of 
U.S. -born MA women had non-Mexican American husbands. However, 
84 percent of these outmarriages were to non-Hispanic White 
males; this was the highest rate for such marriages among the 
Hispanic subgroups examined. Younger wanen were someis^at more 
likely to marry outside their own ethnic group than older wcmen. 
The rate of outmarriage among U.S. -born MA women under 35 years 
old was 19 percent compared to only 13 percent for those aged 35 
and over. The percentage of outmarriages increased substantially 
with increased schooling. For wanen younger than 35, the rate of 
outmarriage among high school graduates was 30 percent compared 
to only 11 percent among those v*io had not ocmpleted high school. 
For women aged 35 and over, the corresponding rates of out- 
marriage were 37 percent among high school graduates and 8 per- 
cent among those >^o had not completed twelfth grade. 
In surrmary, Mexican Americans are becoming an increasingly 
heterogeneous population, both socioeconomically and culturally. 
The majority of Mexican Americans, however, are still located in 
the lower SES strata and have experienced low or intermediate 
levels of acculturation into mainstream (non-Hispanic White) 
American society. 

(Cardiovascular Disease As A Cause of Mortality Amon g Mexican 
Americans 

Two studies have examined the relative importance of car- 
diovascular disease (CVD) as a cause of death among Mexican 
Americans (12,13). One was conducted in California, the other in 
Texas, the two states vrfiere over 86 percent of the nation's 
Mexican American population resides (6). Both studies examined 
mortality data for the period 1969 to 1971. Persons were 
classified as Mexican American or non-Hispanic White using the 
U.S. Census surname identifier. Methodologies differed in that 
the California study compared cause-specific mortality using life 
table deaths conputed for 5-year intervals ages to 85 and stan- 



i 



3 

Rates of outmarriage were based on the Public Use Sample tabula- 
tions for husbands and wives living together at the time of the 
1970 Census enumeration. Rates could be determined for Mexican 
Americans, Puerto Ricans, Cubans, and Hispanos, but not for 
Central and South Americans ( 7 ) . 



370 



dardized death rates directly standardized using the total popu- 
lation of California in 1960; while the Texas study compared only 
standardized death rates directly standardized on the Texas 
non-Spanish surname White fanale age distribution (13). 

The two studies yielded strikingly similar results. Both found 
cardiovascular disease to be the leading cause of death among 
Mexican Mericans, just as it is among non-Hispanic Whites. CVD 
mortality rates were lower for Mexican American males, however, 
than for non-Hispanic White males (in California, 82% of the 
non-Hispanic White rate; in Texas, 85% of the non-Hispanic White 
rate). CVD mortality rates for Mexican American fetvales, on the 
other hand, were virtually identical to those for non-Hispanic 
White fsnales (in (California, 99.8% of the non-Hispanic White 
rate; in Texas, 7% higher than the non-Hispanic White rate). The 
sex differential in CVD mortality was less favorable for Mexican 
American fonales than for non-Hispanic Whites (in California: a 
male-fonale sex ratio of 1.43 for MAs vs. 1.72 for non-Hispanic 
Whites; in Texas, a male-fanale sex ratio of 1.46 for MAs vs. 
1 . 78 for non-Hispanic Whites ) . 

Two other studies have examined secular trends in cardiovascular 
mortality during the first half of the 1970s to determine \/^ether 
Mexican Americans shared in the nation-i^ide decline in CVD mor- 
tality v«*iich occurred during that period (14,15). The first 
study, using data only from Bexar County (San Antonio) Texas, 
found that standardized CVD mortality rates^ f^j- y^g period 1970 
to 1976 declined significantly in both MA men and women and in 
non-Hispanic White males (14). Furthermore, the CVD mortality 
decline in Mexican Artericans was equal to that in non-Hispanic 
v^ites. The second study, using state-wide data from Texas, 
found that standardized proportional CVD mortality rates for the 
period 1970 to 1976 declined in Mexican Americans, but that, par- 
ticularly for MA males, the decline was much less steep than in 
non-Hispanic Whites (15). Each of these studies suffered fron 
the limitation that 1975-76 population denominators were derived 
fron population estimates rather than actual census data. A new 
study, not yet published, vrfiich uses denominators from the 1980 
census for the state of Texas, indicates an interesting sex- 
differential in the rate of CVD mortality decline in Mexican 
Americans during the period 1970 to 1980 (16). The rate of 
decline in Mexican American men was about only half as steep as 
in non-Hispanic Whites, vAiile the rate of decline in Mexican 



4 
Directly standardized to the 1970 U.S. population. 



371 



ftmerican wcmen was one-third to two-thirds steeper than in 
non-Hispanic Whites. 

Socioecononic Status , Accailtur at ion , and Cardiovascular Risk 
Factors in Mexican Americans 

Evidence concerning the level of cardiovascular risk factors in 
Mexican Americans is growing, but research in this area has been 
quite limited over the past 15 to 20 years. This is particularly 
true for research on the association between differences in 
socioeconomic status and acculturation among Mexican Americans 
and the risk of cardiovascular disease. Table 1 provides a list 
of 21 research reports found in a search of the literature for 
the period 1966 to October 1984. These 21 reports are based on 
eight separate studies: 4 carried out on populations in 
California, 3 in Texas, and 1 in the four states along the 
U.S. -Mexico Border. Over half of the reports are fran the San 
Antonio Heart Study (SAHS), a large population-based investiga- 
tion which ccsmpared diabetes and cardiovascular risk factors in 
Mexican Americans and non-Hispanic Whites residing in three 
socioculturally distinct neighborhoods of San Antonio, Texas. 
Almost one-fourth of the 21 reports, including all of those frcm 
the Starr County study, deal exclusively with diabetes or with 
the relationship between diabetes and obesity. Only about half 
of the reports, primarily those frcxn the San Antonio Heart Study, 
examine the relationship between either SES or acculturation and 
cardiovascular risk factors in Mexican Americans. The evidence 
contained in these reports deals with six risk factors: lipids 
and lipoproteins, blood pressure and hypertension, cigarette 
smoking, exercise, obesity, and diabetes. 

1. Lipids and li poproteins . Cholesterol levels in Mexican 
Americans have been examined in five separate studies (17-21). 
All of these ccxnpared cholesterol levels in Mexican Americans 
with those in non-Hispanic Whites. One study looked only at 
very low SES Mexican Americans and found that the age-adjusted 
serum cholesterol levels in Mexican Americans of both sexes were 
higher than those recorded for non-Hispanic Whites in a national 
comparison sample (HANES I ) , vAiich was undoubtedly of hi^er SES 
(17). Two studies used mixed samples v*iich included both lower 
and middle SES Mexican Americans and non-Hispanic Whites, but did 
not carry out stratified analyses or adjust for differences in 
SES between the two ethnic groups (18,19). In one study Mexican 
Americans were predominantly of lower SES, vdiile non-Hispanic 
Whites were predcminantly of middle SES; cholesterol levels were 
no higher in Mexican Americans than in non-Hispanic Whites (18). 
In the other study lower and middle SES subjects were nearly 
equally distributed in the two ethnic groups; cholesterol levels 



372 



in Mexican American men, however, were higher than those in 
non-Hispanic Whites, viAiile cholesterol levels in Mexican American 
women were similar to those in non-Hispanic Whites (19). These 
three studies revealed no consistent pattern of ethnic differen- 
ces in cholesterol levels nor do they permit inferences about the 
relationship between socioeconomic status and cholesterol levels 
in Mexican Americans. Two of the five studies do provide this 
this information; one of these was done in central California 
(20), the other in South Texas (21). 

The California study compared the proportion of hypercholestero- 
lemic males (cholesterol > 260 mg/dl) in six different levels of 
socioeconomic status. The overall prevalence of hypercholestero- 
lemia in Mexican Americans was higher than in non-Hispanic Whites 
(16.7 vs. 13.9%). There was some evidence of an inverse rela- 
tionship between SES and cholesterol levels in non-Hispanic 
Whites, but no evidence of a similar SES gradient in Mexican 
Americans (20). The South Texas study (SAHS) examined cho- 
lesterol as a continuous variable. SES diffrences were examined 
by coitparing cholesterol levels for a random sample of Mexican 
Americans and Non-Hispanic Whites v^o resided in three 
socioculturally distinct neighborhoods of San Antonio, Texas. 
These neighborhoods had been purposively selected by the 
researchers to represent low, middle and high levels of SES and 
acculturation of Mexican Americans, Non-Hispanic Whites were 
sanpled only in the two higher socioeconomic neighborhoods. ^ 
Overall, diolesterol levels tended to be somewhat higher in 
Mexican American than in non-Hispanic White iten, but similar in 
the two ethnic groups for women. Among Mexican Americans, dio- 
lesterol levels were nearly identical in the two lower SES groups, 
but increased markedly and significantly in the high SES group. 
For wanen, on the other hand, cholesterol levels ranained similar 
in all three SES groups. For non-Hispanic Whites, similar sex 
difference was observed in the relationship between socioeconomic 
status and cholesterol. 



5 
Strictly speaking, these neighborhood analyses do not permit a 

clear distinction between emy purely socioeconomic or cultural 
factors vAiich might be operating. Neighborhood differences pro- 
bably reflect the combined effect of socioeconomic status and 
acculturation. Nonetheless, since the three neighborhoods repre- 
sent significantly different levels of socioeconomic status (21), 
the investigators feel justified in referring to the three neigh- 
borhoods as "SES groups." 



373 



In men, cholesterol levels were significantly higher in the upper 
SES group than in the middle group; in wc«nen, cholesterol levels 
were similar for both SES groijips. 

Four studies also examined triglyceride levels (17-19,21). All of 
them found triglyceride levels in Mexican Americans to be higher 
than those in non-Hispanic Whites, although the differences 
tended not to be statistically significant. Ethnic differences in 
triglyceride levels persisted in both sexes even when cotiparisons 
were made within the same SES strata^ ( 21 ) . Among Mexican 
Americans triglyceride levels in men were similar in the two 
lower SES groups, and increased markedly, though not statisti- 
cally significantly, in the highest SES group. In ttecican 
American women, there was a clear tendency for triglyceride to 
decrease in the higher SES group. 

Two lipoproteins were also examined in the San Antonio Heart 
Study: low density lipoprotein cholesterol, associated with 
increased risk of coronary heart disease (CHD) ; and hii^ density 
lipoprotein cholesterol, a protective factor against CHD (21). 
For low density lipoprotein cholesterol (LDL-C)^, the rela- 
tionship with socioecononic status closely paralleled that for 
total cholesterol. In Mexican American men, LDL-C levels were 
similar in the two lower SES groups, but increased markedly and 
statistically significantly in the highest SES group. In 
non-Hispanic men LDL-C also increased significantly frcsn the 
middle to ipper SES group. For wonen in both ethnic groups, on 
the other hand, LDL-C levels were similar in all SES groups. For 
high density lipoprotein diolesterol (HDL-C), there was also a 
sex difference in the relationship with socioeconomic status. In 
men of both ethnic groups HDL-C ranained constant across levels 
of SES. On the other hand, in women of both ethnic groups, HDL-C 



Strictly speaking, these neighborhood analyses do not permit a 
clear distinction between any purely socioecononic or cultural 
factors v^^ich mii^t be operating. Nei^borhood differences pro- 
bably reflect the combined effect of socioecononic status and 
acculturation. Nonetheless, since the three neic^borhoods repre- 
sent significantly different levels of socioeconomic status (21), 
the investigators feel justified in referring to the three neigh- 
borhoods as "SES groups." 

Although SES was not considered, a related report suggests that 
ethnic differences in triglyceride levels persist even v^en 
adjustments are made for a number of relevant behavioral 
variables (i.e., age, obesity, cigarette atnoking, coffee and 
alcohol consumption and, in women, estrogen and oral contracep- 
tive usage) (22) . 



374 



rose significantly with increasing socioecononic status. 
In terms of lipids and lipoproteins, then, it appears that 
increased socioeconomic status may be associated with greater 
protection against CHD in wDmen (i.e., lower triglyceride levels 
and higher levels of HDL-C) , but with increased risk of CHD in 
men (higher cholesterol levels and higher levels of LDL-C) . 

Two other reports f rem the San Antonio Heart Study have examined 
SES differences in dietary practices which may influence serum 
cholesterol (23,24). One report used data frcxn a diet frequency 
questionnaire to devise a scale measuring avoidance of saturated 
fat and cholesterol (23). In Mexican Americans of both sexes, fat 
and cholesterol avoidance increased significantly with increasing 
socioecononic status. Although non-Hispanic Whites in the middle 
SES group still scored significantly higher on the fat avoidance 
scale than Mexican Americans, no ethnic differences were present 
in the highest SES group. No difference in fat avoidance was 
observed between Mexican Americans born in the U.S. and those 
born in Mexico. 

The other SAHS report looked at how well-informed individuals 
were about the role of dietary cholesterol and saturated fat as 
risk factors for cardiovascular disease and at the extent to 
v^ich individuals modified their diet to reduce heart disease 
risk (24). Overall, Mexican Americans were less well-informed 
than non-Hispanic Whites and were less likely to have attempted 
any dietary modifications to reduce risk of heart disease. 
Although increased socioeconomic status was associated with 
increased knowledge and preventive behavior in both ethnic 
groups, the gap in knowledge and behavior between Mexican 
Americans and non-Hispanic Whites began to close at the higher 
SES levels. 

2. Blood pressure and hypertension . Three studies have 
compared blood pressure levels in Mexican Americans and 
non-Hispanic Whites (17-19). All three found diastolic blood 
pressure, in men, and systolic blood pressure, in both men and 
women, to be similar in the two ethnic groups. Two of the stu- 
dies (17,18) found diastolic blood pressure in Mexican American 
women to be lower than in non-Hispanic Whites, v\*iile the third 
found no ethnic differences (19"). The Laredo Project (17) also 
examined prevalence of hypertension in Mexican Americans, using 
two separate definitions utilized in the Hypertension Detection 
and Follow-up Study (HEFP). One definition of hypertension 
("elevated diastolic blood pressure") included only individuals 
with diastolic blood pressures (DBF) greater than or equal to 
95mm Hg. The second definition ("actual" hypertension) included 
individuals with currently elevated diastolic blood pressures 



375 



plus those whose diastolic blood pressures were below 95 imi Hg, 
provided they gave a history of hypertension and were also 
currently taking anti-hypertensive medications. The second defi- 
nition provides for differences in treatment levels vAiich may 
occur across ethnic groups or geographic regions. 

The prevalence of elevated diastolic blood pressure in Laredo 
Mexican Americans (very low socioeconomic status) was compared to 
that of HEFP Whites and Blacks. In Mexican American males the 
prevalence of hypertension was intermediate between those of HEFP 
Whites and Blacks. In Mexican American fennales, on the other 
hand, hypertension prevalence was lower than in either HEFP 
Whites or Blacks. Mexican American males had substantially 
higher rates of elevated diastolic blood pressure in each of 
three age groups (40-49 year olds: 19.4 vs. 7.9%; 50-59 year 
olds: 23.3 vs. 7.1%; 60-69 year olds: 23.8 vs. 5.7%) (17). 
The rate of "actual" hypertension in Laredo Mexican Americans was 
also intermediate between the rates for HEFP Whites and Blacks 
until age 59, after which it became essentially similar to the 
HEFP Black rate. For Mexican American wcmen, however, the rate 
of actual hypertension was slightly hi^er than that in HEFP 
Whites except in the 60-69 year -old age category v*iere the rate 
was as high as that in HEFP Blacks. The large sex differences 
observed for rates of elevated diastolic blood pressure in Laredo 
Mexican Americans were greatly reduced for actual hypertension 
and were, in fact, reversed in the oldest age category (40-49 
year olds: 29.0 vs. 21.1%; 50-59 year olds: 37.2 vs. 26.2%; and 
60-69 year olds: 38.1 vs. 44.3%). The latter finding suggests 
that among Laredo hypertensives, wanen were more likely than men 
to have their hypertension controlled (17). 

SES differences in hypertension prevalence were examined in a 
California study (20) and in the San Antonio Heart Study (21), 
but with two different definitions of hypertension. The 
California study looked at elevated diastolic blood pressure, 
while the SAHS examined actual hypertension. The California 
study found a clear inverse relationship between SES and preva- 
lence of elevated diastolic blood pressure in Mexican American 
males, ranging fran a rate of 8.2 percent in the highest SES 
category to 19.6 percent in the lowest SES category (20). A 
similar SES gradient was present in non-Hispanic Whites. The 
overall prevalence of elevated diastolic blood pressure in 
Mexican American males was 15.6 percent; intermediate between the 
rates found for non-Hispanic Whites and Blacks. 

The San Antonio Heart Study found no SES gradient in prevalence 
of actual hypertension in either Mexican American or non-Hispanic 
White males (26). In Mexican American males, rates of actual 



376 



hypertension were 10.7 percent in the lowest SES group, 7.3 per- 
cent in the middle SES group, and 11.5 percent in the highest SES 
group. The corresponding rates for non-Hispanic White males were 
10.0 percent in the middle SES group and 9.5 percent in the hic^ 
SES group. In contrast to the finding for men, there was a 
strong inverse relationship between socioeconomic status and pre- 
valence of actual hypertension in wcmen of both ethnic groups. 
For Mexican Americans, the rates declined from 9.2 percent in the 
low SES group to 8.4 percent in the middle SES group, and 4.7 
percent in the high SES group; for non-Hispanic Whites, the rate 
declined from 10.7 percent in the middle SES group to 8.7 percent 
in the high SES group. Rates of hypertension appeared to be 
similar in males of both ethnic groups, but lower in Mexican 
American women than in non-Hispanic Whites, although this ethnic 
difference was not statistically significant. Vtien adjustments 
were made for obesity (higher in MAs), Mexican Americans tended 
to have a lower rate of hypertension than non-Hispanic Whites at 
the same SES level. 

Data on the proportion of hypertensives previously diagnosed and 
under treatment with antihypertensive drugs were also reported 
from the San Antonio Heart Study. The proportion of hyperten- 
sives previously diagnosed and under treatment was lower in 
Mexican Americans of both sexes than in non-Hispanic Whites. 
Interestingly, the proportion of previously diagnosed hyperten- 
sives under treatment was as great among low SES Mexican American 
men as high SES men, and actxaally decreased fron the low to high 
SES group in MA wcxnen. Among non-Hispanic Whites, on the other 
hand, there was either no SES difference in the proportion of 
previously diagnosed hypertensives under treatment (for women) or 
the proportion increased with increased socioeconomic status (for 
men). These data suggest that health care deliverers may be par- 
ticularly sensitive to the potential presence of hypertension 
among low SES minorities. Nonetheless, the proportion of Mexican 
American hypertensives both under treatment and under control 
(DBP < 95 m:n Hg) was lower in both sexes at the lower SES levels. 
In addition, lower SES Mexican Americans of both sexes were also 
sonewhat less likely than those at higher SES levels to report 
that they had attempted to control hypertension as a means of 
preventing heart attacks (24). 

The overall proportion of SAHS Mexican Americans under adequate 
control was greater in wcxnen than in men (87 vs. 64 percent). 
Comparable data from the Laredo Study showed 77 percent of MA 
hypertensive wcxnen and only 37 percrent of hypertensive men under 
adequate control (17). While the figures for Mexican American 
women are similar to national figures for hypertension control in 
women, Mexican American men lag far behind national figures for 
hypertension control in nren. 



377 



3. Cigarette annoking . Six studies have conpared smoking 
behavior in Mexican Americans and non-Hispanic Whites 
(18-20,26-28). Overall rates of current snoking appear to be the 
same or higher in Mexican Americans than in non-Hispanic Whites. 
Overall rates, however, obscure an important sex-ethnic interac- 
tion: for males, the proportion of Mexican Americans vfno axe 
current smokers is the same or higher than for non-Hispanic whi- 
tes; for waanen, on the other hand, the proportion of current sno- 
kers is much lower among Mexican Americans than among 
non-Hispanic Whites (19,27,28). Regardless of sex, however, 
Mexican Americans smoke significantly fewer cigarettes per day 
than non-Hispanic Whites (18,27,28). 

SES differences in smoking behavior were examined in three stu- 
dies (20,27,28). One study which included only women found that 
in both Mexican Americans and non-Hispanic Whites, the proportion 
of current smokers decreased with increasing socioeconomic status 
(27). At comparable levels of SES, though, the proportion of 
non-Hispanic White smokers was double that of Mexican Americans. 
Among Mexican Americans, similar proportions of U.S. -born and 
Mexico-born women were current smokers. The central California 
study (20) examined the proportion of heavy cigarette smokers (> 
20 cigarettes per day) among nales only. In both Mexican 
Americans and non-Hispanic Whites, the proportion of heavy smo- 
kers decreased with increasing socioeconomic status. For Mexican 
Americans, the proportion ranged from 6.1 percent in the highest 
SES category to 23.5 percent in the lowest category. For 
non-Hispanic Whites, rates were sonev^^at higher, ranging from 
16.3 percent in the highest SES category to 48.3 percent in the 
lowest . 

Two reports f ran the San Antonio Heart Study compared SES dif- 
ferences in smoking behavior in both men and women. In the first 
report cited, subjects were grouped into two SES categories: low 
and high. Since no low SES non-Hispanic Whites were available in 
the SAHS sample, SES conparisons within ethnic groups could be 
made only for Mexican Americans. For men, the proportion of 
current smokers was greater among Mexican Americans of both SES 
levels than among high SES non-Hispanic Whites. For wcxnen, on 
the other hand, the proportion of current smokers was lower among 
Mexican Americans at both SES levels than among high SES 
non-Hispanic Whites. In Mexican Americans of both sexes the pro- 
portion of current smokers decreased markedly in the higher SES 
group. Within SES levels, the proportion of current smokers was 
twice as high among Mexican American men than among women. Among 
high SES non-Hispanic Whites, on the other hand, a slightly 
higher proportion of watien were current smokers than men. Hi^ 
SES non-Hispanic Whites of both sexes smoked almost twice as many 



378 



cigarettes per day as Mexican Americans in either SES group. 
Among Mexican Americans, high SES men smoked slightly more 
cigarettes per day than low SES men (16.8 vs. 13.3), while 
Mocican American wcxnen in the two SES groups smoked about the 
same number (9.2 cigarettes per day). 

A second SAHS report focussed on how well-informed individuals 
are about the role of smoking as a risk factor for heart disease 
and v*iether they had modified their smoking behavior (i.e., quit 
or never started) to reduce heart disease risk (24). Mexican 
Americans of both sexes tended to be less well-informed about the 
risks of cigarette smoking than non-Hispanic Vftiites. High SES 
Mexican Americans, however, were much better informed on this 
issue than low SES Mexican Americans; ethnic differences in 
knowledge decreased at the higher SES levels. Within the same 
SES level, Mexican American men tended to be better informed 
about the risk of cigarette smoking than women (in the low SES 
group: 10% of men \^. 6% of wcxnen; in the middle SES group, 16 
vs. 18%; and in the high SES group, 31 vs. 26% of wonen). 

For men, about equal proportions of Mexican Americans and 
non-Hispanic vAiites in the middle SES group reported modifying 
their smoking behavior to reduce CHD risk (11% of MAs vs. 12% of 
non-Hispanic Whites); but more non-Hispanic Whites than Mexican 
Americans were likely to report prevention-oriented behavior in 
the high SES group (18% of MAs vs. 24% of non-Hispanic Whites). 
A similar pattern was found for women; in the middle SES group, 
10% of MAs vs. 11% of non-Hispanic Whites reported modifying 
their snnoking behavior cottpared to 16% of MAs and 20% of 
non-Hispanic Whites in the high SES group. Low SES Mexican 
Americans of both sexes lagged far behind in prevention-oriented 
behavior only 6% in both sex groups reported modifying their 
behavior to reduce CHD risk. 

4. Exercise . Three studies have compared the level of phy- 
sical exercise in Mexican Americans and non-Hispanic Whites 
(19,24,27). All three reported a lower level of physical exer- 
cise outside of work in Mexican Americans than in non-Hispanic 
Whites. Only one study (24) examined differences in jiiysical 
exercise by level of SES. Although non-Hispanic Whites were 
generally better informed about- the role of exercise in reducing 
risk of CHD and reported more prevention-oriented behaviors than 
Mexican Americans, both knowledge and preventive-behavior 
increased among Mexican Mericans with increasing SES. For 
women, while only 21 percent of low SES Mexican Americans were 
informed about the role of exercise in reducing CHD risk, 37 per- 
cent cf middle SES wcanen and 52 percent of high SES w:xnen were 
informed on this issue. Similarly, the proportion of Mexican 



379 



American wanen reporting that they engaged in physical exercise 
to reduce risk of heart disease increased from 13 percent in the 
low SES group to 21 percent in the middle group, and 33 percent 
in the high SES group. Even in the highest SES group, though, MA 
wcmen lagged substantially behind non-Hispanic Whites in both 
knowledge and preventive behaviors. For men, the proportion of 
Mexican Americans informed about exercise and CHD rose fron 22 
percent in the low SES group to 40 percent in the middle group, 
and 66 percent in the high SES group. This proportion in high 
SES Mexican American men equalled that observed in high SES 
non-Hispanic Whites. The proportion of Mexican American men 
reporting that they exercised to reduce CHD risk increased frcxn 
18 percent in the low SES group to 28 percent in the middle SES 
group, and 50 percent in the high SES group. Again the propor- 
tion of high SES Mexican American men reporting this prevention- 
oriented behavior equalled the proportion among high SES 
non-Hispanic Whites. On the four risk factors examined in this 
SAHS report (dietary fat, blood pressure, cigarette smoking, and 
exercise), Mexican American men ranked highest on exercise in 
their level of knowledge and prevention-oriented behavior. 

5. Obesity . The available evidence clearly indicates that 
obesity is a major health problem in Mexican Americans, par- 
ticularly among women and those of low socioeconomic status 
(17,18,21,27,30-32). In the Laredo study of very low SES Mexican 
Americans, the age-adjusted prevalence of obesity (defined as 
being 20 percent or more over desirable weight) was 25.8 percent 
in men and 44.8 percent in wcsnen (17). Corresponding figures 
derived from the Health and Nutrition Examination Survey (HANES 
I) for the general U.S. population were only 15.6 percent for men 
and 29.0 percent for women (33). Another study of very low SES 
Mexican Americans in Starr County, Texas, found that the preva- 
lence of obesity (defined as body mass index > 30) was typically 
30 percent or higher in adults of both sexes ( 30 ) . 

Data fron the San Antonio Heart Study found that body mass index 
decreased only slightly in Mexican American men with increasing 
SES, but decreased markedly and significantly in women at each 
higher SES level. Ethnic comparisons within SES-matched strata, 
however, still indicated greater adiposity ainong Mexican 
Alter icans of both sexes than among non-Hispanic Whites (21). 
Comparisons of attitudes and behavior related to obesity in 
middle and high SES subjects revealed that a greater percentage 
of Mexican Americans than non-Hispanic Whites at each SES level 
were likely to express the belief that Americans are too con- 
cerned about losing weight (34). Mexican Americans in both SES 
groups also scored lower than non-Hispanic Whites on scales 
measuring sugar avoidance and dieting behavior, but the ethnic 



380 



differences were statistically significant only for wxnen in the 
middle SES group. Mexican Americans in the high SES group scored 
significantly higher on these scales than those in the middle SES 
group. In non-Hispanic Whites SES differences were statistically 
significant only for men and only for the dieting behavior scale. 

Only one report, also fron the San Antonio Heart Study, examined 
the relationship between acculturation and obesity in Mexican 
Americans (35). Acculturation was measured using a multi- 
dimensional scale v^ich reflected adoption during adulthood of 
non-Hispanic White behaviors, attitudes, and values. Even after 
adjusting for socioeconomic status, increased levels of 
acculturation were found to be associated with significant 
decreases in body mass index in Mexican Americans of both sexes. 
This finding suggests that SES and acculturation may play inde- 
pendent and distinct roles in reducing obesity in Mexican 
Americans. Mechanisms (e.g., diet, exercise, stress, attitudes 
toward obesity) which may mediate the SES-obesity and 
acculturation-obesity relationships are in need of further 
investigation. 

In addition to the role played by overall adiposity, there is 
evidence that the distribution, or patterning, of body fat may be 
an important determinant of sane metabolic disorders (such as 
diabetes) v^ich may be related to heart disease. Limited evi- 
dence, based on subscapular and triceps skinfolds, suggests that 
Mexican Americans have a relatively more central distribution of 
body fat conpared to non-Hispanic Whites (32,36). There is also 
seme data to suggest that the oentrality of the fat distribution 
in Mexican American men increases with increasing SES, while for 
Mexican American wonen centrality decreases (32). Interest has 
been expressed recently as well in the hypothesis that persons 
with upper body obesity have a greater propensity toward metabo- 
lic disorders (e.g. diabetes) than persons with lower body obe- 
sity. While no data are currently available on ethnic 
differences in upper and lower body obesity between Mexican 
Americans and non-Hispanic Whites, the Starr CiDunty study has 
reported that Mexican American diabetics have relatively more 
upper body fat and less lower bcx^ fat than non-diabetics 
(30,31). Data needed to examine ethnic difference in upper vs. 
lower body fat distribution across SES levels are currently being 
collected in the San Antonio Heart Study II. 

6. Diabete s . A recent revise of current research on diabe- 
tes mellitus in Hispanics indicated that the prevalence of 
insulin-dependent diabetes mellitus (IDDM) is less than 5 percent 
and found no evidence for increased prevalence of IDDM in Mexican 
Americans relative to non-Hispanic Whites (37). Non- insulin 



381 



dependent diabetes inellitus (NIDDM) , on the other hand, appears 
to be a major health problan in Mexican Americans, particularly 
those of low socioeconomic status ( 17 , 21 , 37-41 ) . In Laredo , 
Texas, the age-adjusted prevalence of NIDDM in low SES Mexican 
Americans was 15.7 percent in males and 16.1 percent in females 
(17,37); corresponding rates for low SES Mexican Americans in 
Starr County , Texas were 8 . 3 percent in both sexes ( 38 ) . 
Comparisons to the general U.S. population made in both studies 
suggest that low socioeconomic status Mexican Americans are at 
substantially greater risk of NIDDM. 

The San Antonio Heart Study ccxnpared the prevalence of NIDDM 
(defined according to the National Diabetes Data Group (NDDG) 
criteria (42)) in Mexican Americans and non-Hispanic Whites 
across three SES levels (21). In the lowest SES group the age- 
adjusted prevalences for Mexican Americans were ocmparable to 
those reported in the Laredo study: 13.7 percent in males and 
14.8 percent in females. NIDDM prevalence declined in both sexes 
and in both ethnic groups with increasing levels of socioeconomic 
status. In the middle SES group the age-adjusted prevalence for 
males was 14.6 percent in Mexican Americans and 7.0 percent in 
non-Hispanic Whites; the corresponding rates for females were 8.2 
percent in Mexican Americans and 7.3 percent in non-Hispanic 
Whites. In the highest SES group the rates for males dropped to 
6.1 percent in Mexican Americans and 3.6 percent in non-Hispanic 
Whites; for females the corresponding rates fell to 3.7 percent 
in Mexican Americans and 2.2 percent in non-Hispanic Whites. 

Further analyses of the data for Mexican Americans indicates that 
the inverse relationship between socioeconomic status and NIDDM 
may be largely mediated through obesity in MA women, but not in 
men (41). In addition, when SES and acculturation were examined 
separately in relation to NIDDM prevalence, acculturation was 
consistently associated with a reduction in NIDDM prevalence for 
both MA men and women, even after linear adjustments for 
socioeconomic status. The effect of acculturation on NIDDM 
appeared to be largely mediated through obesity in women, but was 
largely independent of obesity in men ( 42 ) . 

Since Mexican Americans tend to be much more obese than 
non-Hispanic Whites, efforts were made to determine v^ether obe- 
sity could explain the excess prevalence of diabetes. Even v^en 
Mexican Americans were closely matched to non-Hispanic Whites on 
degree of obesity, the prevalence of NICCM was significantly 
greater in Mexicans than in non-Hispanic Whites (40). The sum- 
mary prevalence ratio, after matching for obesity, was 2.54 for 
men and 1.70 for wcmen. While obesity contributes to NIDDM in 
Mexican Americans, particularly Mexican American wcanen, it does 



382 



not entirely explain the excess prevalence rate that has been 
observed relative to non-Hispanic Whites. 

There is limited evidence to suggest that the excess NIDDM preva- 
lence in Mexicans v\*iich cannot be attributed to obesity may have 
a genetic component related to degree of native American admix- 
ture. In the San Antonio Heart Study NIDDM prevalence in Mexican 
Americans was intermediate between the rates observed for the 
predominantly non-Hispanic White HANES II population (3.1%), 
which presumably has few if any native American genes, and for 
Pima Indians (49.9%), who are believed to have close to 100 per- 
cent native American genes (39). NIDDM prevalence for 
non-Hispanic Whites in the SAHS sample was nearly identical to 
that observed for the HANES II population (3.0%). In addition, 
the stepwise decline in NIDDM prevalence f rem the low to high 
Mexican American SES groups observed in the San Antonio Heart 
Study was paralleled by a similar stepwise decline in percent 
native American admixture (39,43). Low SES Mexican Americans had 
about 46 percent native American admixture, MAs middle SES 
Mexican Americans about 26 percent native American admixture, and 
high SES Mexican Americans about 18 percent native American 
admixture. It should be kept in mind, however, that this evi- 
dence is currently ecological in nature, although more definitive 
studies are now in progress. 

Suimary and Recatmendations 

This review confirms that the profile of cardiovascular risk fac- 
tors is less favorable in Mexican Americans than in non-Hispanic 
Whites. Within the Mexican American population, those in the 
lowest socioeconomic group and those v^o are the least 
acculturated have a significantly worse profile of cardiovascular 
risks than those in higher socioeconanic groups and those who are 
more acculturated. Obesity and non-insulin dependent diabetes 
mellitus rank as major health problans in Mexican Americans of 
both sexes. For Mexican American males, hypertension and 
cigarette smoking rank as significant health problems, as well. 
Finally, the less favorable profile of lipids and lipoproteins in 
Mexican Americans (greater hypertriglyceridemia and lower levels 
of high density lipoprotein cholesterol in both sexes; and 
greater hypercholesterolania and higher levels of low density 
lipoprotein cholesterol in males) relative to non-Hispanic Whites 
should also be recognized as a public health concern. In light 
of these findings, the following recatmendations sean warranted: 

1. Major priority should be given to public health ini- 
tiatives directed toward reducing the high rates of obesity and 
non-insulin dependent diabetes mellitus in the Mexican American 



383 



population. Toward this end, research itonies should be 
appropriated to determine vi^ether genetic as well as lifestyle 
factors are related to excess NIDDM prevalence in Mexican 
Americans . 

2. Eiducational programs and improvements in health care 
delivery should be directed toward increasing compliance with 
antihypertensive regimens and reducing the rate of current 
smoking in Mexican Merican males. 

3. Health care deliverers should be alerted to the need for 
careful monitoring of lipids and lipoproteins in Mexican 
Americans associated with increased risk of coronary heart 
disease. This seems particularly important in low SES Mexican 
Americans of both sexes and in upwardly mobile Mexican American 
males. 

4. Public health initiatives to lower the profile of coro- 
nary risk in Mexican Americans should be directed primarily 
toward those at lower levels of socioeconomic status. However, 
since Mexican Americans at all SES levels tend to lag behind 
non-Hispanic Whites in levels of knowledge and behavior related 
to the prevention of coronary heart disease, educational programs 
designed to reduce CHD risk should be directed toward Mexican 
Americans at all socioeconomic levels. 



384 



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22. Haffner SM, Knapp JA, Stern MP, Hazuda HP, Rosenthal M, 
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24. Hazuda HP, Stern MP, Gaskill SP, Haffner 34, Gardner LI: 
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25. Stern MP, Gaskill SP, Allen CR Jr, Garza V, Gonzales JL, 
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26. Franco U, Stern MP, Rosenthal M, Haffner SM, Hazuda HP, 
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29. Haffner S, Rosenthal M, Hazuda H, Stern M: Cigarette 
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32. Malina RM, Little BB, Stern MP, Gaskill SP, Hazuda HP: 
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35. Hazuda H, Haffner S, Stern M, Rosenthal M, Franco L: 
Effects of acculturation and socioeconomic status on obesity 
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39. (Gardner LI Jr, Stern MP, Haffner SM, Gaskill SP, Hazuda HP, 
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390 



Ischemic Heart Disease 
Risk Factors in Hispanic 
Americans 



Shiriki K. Kumanyika, Ph.D. M.P.H. 

Department of Epidemiology 

Johns Hopkins School of Hygiene and Public Health 

Baltimore, Maryland 

Daniel D. Savage, M.D., Ph.D. 

Medical Advisor 

National Center for Health Statistics 

Hyattsville, Maryland 



TABLE OF CONTENTS 

1.0 INTRODUCTION 394 

2.0 ISCHEMIC HEART DISEASE RISK FACTORS AMONG MEXICAN AMERICANS 

AND HISPANIC-HERITAGE POPULATIONS IN THE SOUTHWEST . . . .395 

2.1 Elevated Blood Pressure and Hypertension 

2.2 Cholesterol 

2.3 Cigarette Smoking 

3.0 ISCHEMIC HEART DISEASE RISK FACTORS AMONG PUERTO RICANS . . .405 

3.1 Data Issue 

3.2 Ischemic Heart Disease Risk Patterns 

4.0 SUMMARY 407 

5.0 REFERENCES 408 

6.0 SUPPLEMENTARY REFERENCES 410 



393 



1.0 INTRODUCTION 

This paper presents selected data on three of the standard ischemic 
heart disease (IHD) risk factors (hypertension, elevated cholesterol, and 
cigarette smoking) among Hispanic Americans. In addition to the material 
presented here, the Cardiovascular Diseases Subcommittee report analysis of 
IHD risk among Hispanics draws upon information compiled by Hector F. 
Meyers, Ph.D., one of the subcommittee's consultant writers, and upon the 
commissioned paper by Hazuda on socioeconomic factors and CVD (1) . 
However, in their entirety, the data available at the time of the Task 
Force deliberations do not provide an adequate picture of IHD risk patterns 
among Hispanics --either in the aggregate, according to ethnic-regional 
subgroups, or according to sociocultural and socioeconomic distinctions 
which may have a direct bearing on IHD risk. 

Some mortality, morbidity and risk factor data which relate to 
Hispanics are inaccesible in that they are grouped within data for 
"non-whites". "Spanish-surname" tabulations are ambiguous as to the 
homogeneity of the population so classified, and the ethnicity of 
"Spanish-surname" populations must be inferred on a geographical basis. 
For example, according to Aday et al. (2), 83% of a southwest Spanish 
surname sample drawn for a 1975-76 national survey were Mexican American 
persons (Colorado, Texas, New Mexico, Arizona, and California were the 
sample states). In the New York City area, most Spanish-surname persons 
are Puerto Rican. In Florida, most are Cuban Americans. Other 
Spanish-surname persons have origins in Central or Latin America or other 
Spanish-speaking areas of the world. 

The numbers of Hispanic respondents in health surveys of the overall 
United States population (e.g., the National Health and Nutrition 
Examination Survey (NHANES) and the National Health Interview Survey 
(NHIS)) have been small, proportional to the relatively small numbers of 
Hispanics in the population. However, the Hispanic Health and Nutrition 
Examination Survey (HHANES) , to be completed in 1985, has been specially 
designed to provide data on a range of health status variables for 
sizeable, representative samples of Mexican Americans, Puerto Ricans , and 
Cuban Americans (3). HHANES will become the appropriate reference point for 
many IHD risk factor considerations related to Hispanic populations after 
late 1985 or early 1986. 

Most of the information in this paper relates to Mexican Americans and 
Hispanics in the Southwest who are presumed to be primarily Mexican 
Americans. This information is presented, by risk factor, in section 2. 



394 



Section 3 includes relatively brief comments related to the assessment of 
IHD risk among Puerto Ricans . Essentially no relevant data on Cuban 
Americans were identified. 



2.0 ISCHEMIC HEART DISEASE RISK FACTORS AMONG MEXICAN AMERICANS 

AND HISPANIC-HERITAGE POPULATIONS IN THE SOUTHWEST 

2.1 Elevated Blood Pressure and Hypertension 

Kraus et al. (4) reported the prevalence of elevated blood pressure 
(DBF >=95 mm Hg) for Hispanic men screened at the University of California 
Multiple Risk Factor Intervention Trial (MRFIT) center during 1975-76. The 
approximately 19,000 screenees included 738 Spanish American men: 340 and 
398 in the 35-44 and 45-57 year age-groups, respectively. In the white 
comparison group, a higher proportion of white men were in the 45-57 year 
age-group compared to the Spanish American men. The prevalences of 
elevated blood pressure among Spanish American men and white men are 
compared in Table 1, overall and according to categories of a 77 point 
education-occupation scale of socioeconomic status. 



Table 1: Prevalence of elevated blood pressure among Spanish American 
and white men in the U.C. Davis MRFIT screenee population, 
overall and according to socioeconomic status (SES). Elevated 
blood pressure is defined as diastolic blood pressure > or = 95 
mm Hg) (from 4; Table 3) 

SES Spanish White 

American 

% % 

11.7 

9.0 
10.8 
12.0 
13.1 
14.7 
16.1 



The data in Table 1 indicate an overall higher prevalence of elevated 
blood pressure among the Spanish American men. High blood pressure 
prevalence increases with decreasing socioeconomic status among the men in 
both ethnic groups. The excess prevalence among the Spanish American men 
is most evident in the lower SES strata. The black men in this population 
had the highest prevalence of elevated blood pressure of all the ethnic 
groups reported (18.8% prevalence), but did not show the SES gradient. 



all SES 




15.6 


11-21 


high 


SES 


8.2 


22-32 






- 12.3 


33-43 






11.5 


44-54 






17.4 


55-65 






19.1 


66+ 


low 


SES 


19.6 



395 



Data for Hispanic men and women in California relating to several 
hypertension variables are included in the report of the California 
Hypertension Survey. This survey, conducted in 1979, used a multistage, 
random, probability sample of households. The Hispanic sample included 
1,647 persons. The survey results on hypertension prevalence, awareness, 
treatment and control for Hispanic men and women in two age-groups are 
shown in Table 2. 



Table 2. Hypertension variables for Hispanic men and women- 
California Hypertension Survey (from reference 5; Tables 
4.3 and 4.4.) Comparison data for white respondents in 
the same survey are shown in brackets. 





H; 


Lspanic 


Hispanic 


Hispanic 


Hispanic 




Men 18- 


•49 


Men 50+ 


Women 


18-49 


Women 50+ 


% hyperten 




14.1 




39.4 


7.6 




44.7 


(140/90+ or 


[ 


16.3 




45.6 


6.4 




46.7 ] 


on meds) 
















%140/90+ 




13.9 




35.7 


6.9 




29.4 




[ 


15.0 




38.5 


4.8 




36.4 ] 


7a hyperten 




28 




64 


45 




68 


aware 


[ 


42 




60 


61 




70 ] 


% hyperten 




6 




38 


20 




55 


on drug Rx 


[ 


15 




40 


41 




52 ] 


% hyperten 




1 




7 


8 




27 


controlled 


[ 


7 




15 


26 




21 ] 



Among men, the prevalence of hypertension by either of the criteria 
shown is somewhat lower among Hispanic vs . whites in both age-groups . 
Awareness, treatment, and control are lower among Hispanic men compared to 
white men in the younger age-group. Among the older men (aged 50 or over), 
hypertension awareness is slightly higher among Hispanics but treatment and 
control are somewhat lower among Hispanics, compared to whites. Among 
women, the prevalence of hypertension is higher in Hispanic women than in 
white women in the younger age-group but somehwat lower in the older 
age-group. Younger Hispanic women are less aware and less likely to be 
treated and controlled than their white counterparts. For older women, 
the treatment and control appear to be somewhat better among Hispanic than 
among white women. 



396 



In comparisons of overall hypertension rates among the ethnic groups 
surveyed, adjusting for differences in the age, sex, and body weight 
distributions of the populations being compared, the prevalence of 
hypertension (systolic blood pressure >140 mm Hg or diastolic blood 
pressure >90 mm Hg or on medication) was 21.5% among Hispanics , compared to 
23.4% among whites and 35.2% among blacks (5; Table 4.2). The adjusted 
mean levels of systolic and diastolic blood pressure among Hispanics and 
whites were not markedly different (e.g., Hispanics mean DBP was 74.9 
compared to 76.4 for whites). 

Additional probability sample data which permit comparisons of blood 
pressure levels among Mexican Americans and whites have been reported from 
cycle 1 of the NHANES. These comparison data are shown in Table 3, for 
men, and Table 4 for women. 



Table 3. Systolic and diastolic blood pressure levels of Spanish*/ 
Mexican American men, with comparison values for white 
men, U.S., 1971-1974, NHANES I. (from reference 6; 
Tables 25 and 27). 





SYSTOLIC (mm Hg) 


DIASTOLIC (mm 


Hg) 


AGE- 


Spanish/ 




Spanish/ 




GROUP 


Mex American 


White 


Mex American 


White 




Men 


Men 


Men 


Men 


18-24 


119.1 


123.7 


73.4 


76.4 


25-34 


121.6 


125.2 


78.4 


80.8 


35-44 


124.7 


127.0 


81.8 


84.2 


45-54 


140.1 


134.7 


86.5 


87.5 


55-64 


139.9 


139.6 


86.8 


86.4 


65-74 


146.0 


146.0 


82.4 


84.9 



examinees who identified themselves as Spanish Americans or 
Mexican Americans 



397 



Table 4. Systolic and diastolic blood pressure levels of Spanish"/ 
Mexican American women, with comparison values for 
white women, U.S., 1971-1974, NHANES I. (from 
reference 6; Tables 25 and 27). 



SYSTOLIC (mm Hg) 



DIASTOLIC (mm Hg) 



AGE 


Spanish/ 




Spanish/ 




GROUP 


Mex American 


White 


Mex American 


White 




Women 


Women 


Women 


Women 


18-24 


109.6 


115.1 


67.1 


71.3 


25-34 


117.2 


116.2 


74.4 


74.6 


35-44 


122.4 


122.6 


78.3 


79.3 


45-54 


130.0 


131.1 


83.7 


82.6 


55-64 


144.8 


143.0 


85.8 


86.2 


65-74 


150.1 


151.6 


81.6 


85.4 



" examinees who identified themselves as Spanish American or 
Mexican American. 



Among men in the NHANES I sample (Table 3), systolic blood pressures of 
the Spanish/Mexican American men were lower than those of white men between 
the ages of 18 and 44 but comparable to or higher than those of white men 
in the 45-74 year age-groups. Diastolic blood pressures of the Hispanic 
men were comparable to or somewhat lower than those of their white 
counterparts. Among women (Table 4), systolic and diastolic blood presures 
of the Spanish/Mexican American women were generally similar to those of 
white women, slightly lower in several of the age groups. 

Christensen et al . (7) reported blood pressure levels of Mexican 
American and Anglo students (mean age 16 years) and parents (mean ages 46 
and 43 years for fathers and mothers) from the Houston-Baylor Prevalence 
Study. Data are for the 1972-75 period. The number of Mexican American 
parents who participated was small. Data for Mexican Americans were 
reported for 165 male and 169 female students but only 44 fathers and 80 
mothers . Among Anglos there were 500 to 600 in each of the four categories 
(i.e., male and female students and parents). 

Mean systolic and diastolic blood pressure levels for Mexican American 
and Anglo fathers were almost identical (e.g. ,mean systolic blood pressures 
were 126.6 mm Hg and 126.9 mm Hg for Mexican American and Anglo fathers, 
respectively. Mean systolic and diastolic blood pressures of Mexican 
American and Anglo male students were similar also--120.2 mm Hg systolic 
for Mexican American boys vs. 118.7 mm Hg for white boys. Blood pressure 
levels of the Mexican American mothers were higher than those of the Anglo 
mothers--125 . 1 mm Hg systolic for Mexican American mothers compared to 118.2 
mm Hg systolic for Anglo mothers; 80.5 mm Hg diastolic vs. 76.7 mm Hg 
diastolic for Mexican American mothers vs. Anglo mothers. Blood pressure 



398 



levels of the Mexican American girls were approximately 2 mm Hg lower than 
those of Anglo girls (109.6 vs. 111.3 mm Hg systolic and 68.6 vs. 70.4 mm Hg 
diastolic) . The large standard deviations and the lack of adjustment for 
age or body weight limit the ability to interpret these small differences. 

Stern et al. (8) reported blood pressure levels from a 1979 
cardiovascular survey of Mexican Americans in Laredo, Texas. Eighty-eight 
percent of 462 age-eligible Mexican Americans participated (the age range 
was 40 to 74 years of age) . Mean systolic and diastolic blood pressure 
levels of the "Laredo Project" men and women were consistently lower than 
the NHANES I levels for black men and women in all sex -age -groups (men and 
women between 40 to 74 years) . Compared to NHANES I data for whites and 
Spanish/Mexican Americans (shown in Tables 3 and 4 above), mean systolic 
blood pressure levels for Laredo Project men and women were lower in some 
age-sex groups and higher in other groups (8; Tables 1 and 2). 

The prevalence of hypertension (i.e., medication for hypertension 
and/or uncontrolled high blood pressure taken together) among Mexican 
Americans was estimated to be higher than among whites but lower than among 
blacks, using estimates for the Hypertension Detection and Follow-up 
Program (HDFP) as the comparison data--but only in the 40 to 59 year olds. 
Hypertension prevalence rates among Mexican Americans in the 60-69 year 
age-group were equal to the high levels reported for blacks. Hypertension 
prevalences for Laredo Mexican American men ages 40-49 and 60-69 years were 
29 and 38% respectively, compared to estimates of 20.6% and 18.5% 
respectively for HDFP white men and 39% and 36.3%, respectively for HDFP 
black men. The same data for women- -Laredo: hypertension prevalences of 
21.1% and 44.3% for 40-49 and 60-69 year old Mexican American women, 
compared to 18.0% and 23.6% estimated for HDFP white women and 40.8% and 
42.1% for HDFP black women (8, Table 4). Stern et al. (8) note that this 
intermediate blood pressure prevalence status of Mexican Americans in 
Laredo (between levels for blacks and whites) is similar to the findings of 
Kraus et al. (4) among the MRFIT screenees. Hypertension awareness, 
treatment and control levels were greater among Laredo women than men in 
every age category. In addition, Laredo project women appeared to have 
better awareness, treatment^ and control than white or black women in a 
comparison group (Impact of Hypertension Information (IHI) Program; 
reference 9). Laredo Project men were somewhat less likely than white or 
black men in the IHI population to be aware, treated or controlled. 

Overall, these data on blood pressure levels and hypertension 
prevalences among Hispanics are very difficult to interpret. Variances 
around mean levels reported are often large and relevant tests of 
statistical significance are not reported. Comparison data for some reports 
are taken from external sources; thus situational or methodologic 
differences across studies may affect results. The SES and weight effects 
on blood pressure may contribute to the discrepancies in the results. With 
these considerations in mind, it seems safe to infer that the problem of 
hypertension among Mexican Americans and Hispanics in the southwestern 
United States is generally not of the same magnitude reported for U.S. black 
populations overall, although it may be substantial, and greater than for 
whites, among certain subgroups. 



399 



2.2 Cholesterol 

Kraus et al. (4) reported a 16.7% prevalence of elevated serum 
cholesterol (defined as > or = 260 mg/dl) for the Spanish American men in 
the MRFIT screenee population described above, compared to 13.9% prevalence 
among the white men. Prevalences of elevated cholesterol by socioeconomic 
status subgroup are shown in Table 5. The prevalence of elevated 
cholesterol among Spanish American men is higher than for white men in all 
SES classes. The direction or nature of the SES-cholesterol relationship, 
if any, within these two ethnic groups is not clear, although a U-shaped 
relationship is suggested. 



Table 5: Prevalence of elevated serum cholesterol among Spanish American 
and white men in the U.C. Davis MRFIT screenee population, 
overall and according to socioeconomic status (SES) (from 4; 
Table 3) 

SES Spanish White 

American 

% % 

13.9 

12.5 
14.1 
14.4 
13.9 
15.4 
16.1 



The Houston-Baylor Prevalence Study data reported by Christensen et 
al. (7) also compared plasma cholesterol levels of Mexican American and 
Anglo parents and children. There were no differences between Mexican 
American vs. white students of either sex. Among the adults, the 
Mexican American men had cholesterol levels higher than either white or 
black fathers (Mexican American fathers: 218 mg/dl; white fathers: 210 
mg/dl; black fathers: 209 mg/dl). Mexican American mothers had the lowest 
cholesterol levels of the three groups (Mexican American mothers: 192 
mg/dl; white mothers: 198 mg/dl; black mothers: 200 mg/dl). As noted 
earlier when reporting the blood pressure findings from this study, the 
differences reported cannot be interpreted in light of the large standard 
deviations and lack of age or relative weight adjustments. It should also 
be noted that the overall cholesterol values in Houston were notably lower 
than values reported in national surveys. Even with consideration of 
methodological differences in cholesterol determinations, Houston values 
were probably 15mg% lower than in NHANES I. 



all SES 


16.7 


11-21 high SES 


20.4 


22-32 


18.5 


33-43 


17.2 


44-54 


14.0 


55-65 


17.8 


66+ low SES 


19.6 



400 



Fortmann et al. (10) report plasma cholesterol levels at baseline in 
the Stanford Three Community Study and report changes in cholesterol levels 
after the 1972-1975 intervention period. The three communities were 
semi-rural agricultural communities. The Hispanic persons surveyed were 
classified as either bilingual or Spanish-speaking. Five classes of the 
Hollingshead SES index are reported for stratification of results; however, 
the Hispanic persons are almost all confined to the two lowest categories 
(70 out of 80 bilingual persons and 51 out of 52 Spanish-speaking, with 45 
of the Spanish-speaking in the lowest category) . The only useful 
comparison seems to be of baseline plasma cholesterol levels across ethnic 
groups within the lowest category (class 5). Within SES class 5, plasma 
cholesterol levels were lowest in the Spanish-speaking group (199 mg/dl), 
intermediate in the bilingual group (210 mg/dl) , and highest among Anglo 
persons (220 mg/dl) (10; Table 1). 

Stern et al. (11) compared levels of serum cholesterol in the Laredo, 
Texas population (described earlier) to cholesterol levels of the Lipid 
Research Clinics' population (comparison data were from reference 12). The 
values reported are shown in Table 6. 



Table 6: Serum cholesterol levels of Laredo Project Mexican American men 
and women with comparison data for white men and women in the 
Lipid Research Clinics (LRC) population (from 11; Table 5). 

Mexican Mexican 

American American 

Age Men White Men Women White Women 



Mean cholesterol levels (mg/100 ml) 



40-44 


241.8 


206.5 


45-54 


220.4 


212.4 


55-64 


224.9 


213.6 


65-74 


207.1 


210.9 



215.5 


194.5 


218.5 


210.9 


234.6 


227.2 


238.6 


228.5 



The prevalence of obesity in this Mexican American population was 
intermediate between levels reported for U.S. whites and Pima Indians. 
Prevalence of hyperglycemia was also intermediate between whites and Pima 
Indians and this was apparently not due to differences in the % of 
diabetics controlled. With the exception of 65-74 year old men, the serum 
cholesterol levels of Mexican Americans were somewhat higher than those of 
the LRC whites. 

Stern et al. (13) reported total and HDL cholesterol and related 
variables in Mexican and Anglo men and women in San Antonio Texas (San 
Antonio Heart Study) . The major purpose of this report was to look at 
effects of cultural and socioeconomic status on these variables. However, 
ethnic comparisons were briefly discussed. The prevalence of diabetes 



401 



among Mexican American men was twice that of Anglo men. It was also 
somewhat higher in Mexican American women vs. Anglo women. The prevalence 
of obesity was consistently higher in Mexican Americans vs. Anglos--in 
both sexes. HDL cholesterol levels were consistently lower in Mexican 
Americans in both sexes. No consistent patterns of ethnic differences in 
total cholesterol were observed. 

Overall, no consistent pattern of Hispanic-white cholesterol 
differences can be inferred from these data. As noted earlier regarding 
findings on blood pressure, some of the inconsistencies may be due to 
weight and SES differences across comparison groups. 



2.3 Cigarette Smoking 

Samet et al. (14) reported smoking data from a survey in Bernillo 
County, New Mexico. The survey was conducted around 1980. Data were 
collected through mailed questionnaires supplemented by telephone and 
home interviews to increase response rates. Response rates were 
75-78% for Anglo men and women; 60 to 69% for Hispanic men and women. 
The Hispanic sample was of lower SES than the Anglo sample. Thus, it 
is not possible to separate ethnic and socioeonomic effects in the 
smoking data. 

Comparable smoking patterns (current, former, never smoked) were 
observed in Hispanic and Anglo samples except that among 40-59 year 
old Anglo men the proportion of ex-smokers was higher than the 
proportion of ex-smokers among Hispanic men. The cumulative cigarette 
exposure was lower among Hispanics due to fewer average cigarettes smoked, 
not shorter smoking duration. 

Smoking data for Hispanics (unspecified) and whites are given in 
an Advance Data report from the National Center for Health Statistics 
(15). Preventive health practices were surveyed in a 1977 National 
Health Interview Survey. Age-, sex-, and ethnic-specific tables are not 
given. Data are shown in Table 7. A larger proportion of Hispanics than 
whites had never smoked, although the percentages of current smokers were 
similar. A substantially larger percentage of Hispanic than white smokers 
reported smoking less than 15 cigarettes per day. 



402 



Table 7. Reported smoking status of Hispanics and whites in a 1977 
National Health Interview Survey (from reference 15) 

Average # cigs/day 
for smokers 
<15 >25 

25.2 29.8 

59.1 13.6 



Never 


Former 


Current 


Smoked 


Smoker 


Smoker 


% White 43 . 1 


21.7 


35.2 


% Hispanic 54.1 


12.3 


33.5 



403 



Roberts and Lee (16) reported smoking data from the Human Population 
Laboratory Studies (1974 and 1975). Households in Alameda County, 
California census tracts were sampled (Table 8). In the 1975 sample, which 
was much smaller than the 1974 sample, there is an impression that Chicanos 
smoke less than whites. Smoking patterns of the two groups appear 
comparable in the 1974 data. Multivariate analyses controlling for age and 
education or income clarified the ethnic differences such that the authors 
concluded that Chicano rates of "never smoking" were higher than for Anglos. 



Table 8: Smoking behavior of Chicanos and Anglos in Alameda County 
in two survey samples (from 16; Table 2) 





n 


current 


former 


never 


1974 










White 


2292 


34.3 


22.5 


43.2 


Chicanos 


162 


36.0 


16.8 


47.2 


1975 










White 


346 


45.1 


17.7 


37.2 


Chicanos 


225 


36.2 


16.5 


47.3 



Smoking patterns among Spanish American and white MRFIT screenees in 
California are shown in Table 9. Spanish American men smoke less than white 
men in all SES strata. The prevalence of smoking 20 or more cigarettes 
per day decreases with increasing SES (4) . 



Table 9: Percentages of Spanish American and white U.C. Davis MRFIT 
screenees smoking 20 or more cigarettes per day, overall and by 
socioeconomic status (from 4; Table 3). 



SES 



Spanish 
American 



White 



all SES 


20.7 


11-21 high SES 


6.1 


22-32 


10.8 


35-43 


21.7 


44-54 


22.0 


55-65 


25.7 


66+ low SES 


23.5 



30.2 

16.3 
25.6 
32.6 
36.7 
42.2 
48.3 



404 



Smoking status data for Hispanic men and women in the California 
Hypertension Survey population are shown in Table 10. Rates of current and 
former smoking are similar among Hispanic and white men, although Hispanic 
men smoke fewer cigarettes per day. Among women, all smoking variables are 
lower among the Hispanic women. Hispanic men who smoke may be less likely 
to want to quit than white men, in both age-groups. Younger Hispanic women 
smokers appear to be more likely to want to quit than white women in this 
age-group. 



Table 10: Cigarette Smoking Variables among Hispanic American men and women 
in the California Hypertension Survey, 1979 (from reference 5; 
Table 7.5). Comparison data for whites are shown in brackets 



% current regular 
smokers 

% current or 
former smokers 

average cigarettes 
per day among 
current smokers 



% of current smokers 

who would like to quit [ 71.0 



Men 


Men 


18-49 


50+ 


38.8 


34.0 


[34.6 


30.5 


58.1 


73.6 


[ 58.0 


72.6 


17.7 


16.7 


[ 26.5 


28.3 


66.3 


50.8 


[ 71.0 


59.0 



Women 


Women 


18-49 


50+ 


21.3 


20.2 


36.5 


25.9 ] 


37.1 


37.2 


52.2 


48.7 ] 


9.7 


16.4 


23.4 


23.2 ] 


72.3 


57.9 


63.8 


60.8 ] 



Overall, the smoking data are relatively consistent in showing lesser 
smoking prevalences and less heavy smoking among Hispanics when compared to 
whites, particularly when SES factors are controlled. 



3.0 ISCHEMIC HEART DISEASE RISK FACTORS AMONG PUERTO RICANS 

3.1 Data Issue 

A recently published paper by Rosenwaike and Preston (17) questioning 
the validity of age-reporting in some data for Puerto Ricans may be of 
interest regarding the interpretation of mortality patterns for this group. 
The authors note that recent official statistics show a longer 
life expectancy among both males and females in Puerto Rico compared to 
that for males and females in the United States (and all but a few other 
countries). They suggest, however, that there appears to be strong 
evidence of widespread overstatement of age among Puerto Ricans at the 
older ages, resulting in an underestimation of mortality rates. 



405 



Table 1 in the Rosenwaike and Preston paper (17) notes life 
expectancies after age 45 (1969-71) of 30.3 for Puerto Rican men vs. 27.5 
and 24.6 for mainland white and non-white men. For Puerto Rican women the 
life expectancy after age 45 years is 34.2 years vs. 33.5 and 29.8 for 
mainland whites and non-whites. The authors present several graphs and 
tables which demonstrate an excess of "age-heaping" (tendency to report 
ages with terminal digits of zero and five) in the distribution of ages 
among Puerto Ricans over age 40. Also, there is some inconsistency in the 
data from successive censuses regarding the numbers of persons at different 
ages. In discussing this analysis, the authors note that an overstatement of 
one year would introduce a 10% error and two years a 20% error. 

3.2 Ischemic Heart Disease Risk 

Nearly all of the papers on IHD in Puerto Ricans are for the San 
Juan area. Gordon et al. have published two reports (18,19) 
comparing men in Framingham, Honolulu, and Puerto Rico. Some baseline data 
from this comparison are shown in Table 11. The Puerto Rican men have lower 
levels in all IHD risk factor and morbidity categories except diabetes. 



Table 11: Baseline data for Puerto Rican and Framingham men on IHD risk 
variables (from reference 18; Table 2) 



Relative weight (%) 

SBP (mm Hg) 

DBP (mm Hg) 

Serum cholesterol (mg%) 

i^ cigarettes/day 

diabetes by Hx 

LVH-ECG 

Smokers 

Angina Pectoris 

Coronary Insufficiency 

Myocardial Infarction 

" difference is 25mg% for Puerto Ricans after adjustment for laboratory 
differences) 



At two-year follow up (18), Framingham men were reported to have a 
two-fold greater risk of coronary heart disease (CHD) than men in 
Puerto Rico, even after adjustments for blood pressure and cholesterol. The 
differences in rates between Puerto Rican men and Framingham rates were 
small or nonexistent in younger men and larger in the older men. The 
apparent absence of a smoking effect on CHD among Puerto Rican men was 
noted as an important exception to the overall pattern of similar risk 
factor/outcome associations across ethnic groups (19). Most risk 



FRAMINGHAM 


PUERTO RICO 


120.04 




112.50 


136.41 




130.35 


85.07 




82.19 


233.96 




202.45* 


12.26 




7.63 


percent 


of group 




3.7 




5.3 


2.3 




1.5 


57.7 




44.4 


3.8 




1.3 


0.5 




0.5 


1.2 




0.1 



406 



factor/outcome associations were generally similar in all three cohorts in 
spite of lower overall risk in the Honolulu Japanese and Puerto Rican 
cohorts compared to Framingham. However, a later analysis of the Puerto 
Rican Heart Program data using 8 year incidence (which gave a larger number 
of incident cases) established an association of smoking with increased 
incidence of myocardial infarction in both urban and rural Puerto Rican men 
(20). This association was not found with other CHD endpoints. 



4 . SUMMARY 

Available data on patterns of IHD risk among Mexican Americans and 
Puerto Ricans are limited. Data relating to Cuban Americans appear to be 
lacking. Data from the HHANES, which will describe all three groups, are 
not yet available. Concurrent data for whites will not be available for 
comparison with HHANES; however, older data from NHANES II are available for 
comparison. A comparison of age-adjusted heart disease mortality in 
predominantly Hispanic census tracts in Los Angeles with rates of Los 
Angeles whites, gives the impression that Hispanics are at lower risk of 
dying of heart disease than whites (21). Levels of smoking appear to be 
lower in Hispanic populations. Available data on other IHD risk factors do 
not clearly establish whether levels for Hispanics are lower, higher, or 
variable in relation to those of whites. Analyses are needed which examine 
risk factor patterns within cultural and SES subgroups of Hispanics and 
also adjust for levels of overweight and diabetes. 

ACKNOWLEDGEMENTS 

We gratefully acknowledge the editorial assistance of Sandra 
J. Anderson and Elisabeth Pitt. 



407 



5 . REFERENCES 

1. Hazuda HP. Differences in socioeconomic status and acculturation 
among Mexican Americans and Risk of Cardiovascular 

Disease. Background paper prepared for the Secretary's Task Force 
on Black and Minority Health. 1984. 

2. Aday LA, Chiu GY, Andersen R. Methodological issues in 
health care surveys of the Spanish heritage population. 
Am J Pub Health 1980;70:367-374. 

3. Transcript of remarks by Fernando M. Trevino, Ph.D., M.P.H. 
to the Secretary's Task Force on Black and Minority Health. 
National Institutes of Health. Bethesda, MD. August 8, 1984. 

4. Kraus JF, Borhani NO, Franti CE. Socioeconomic status, 
ethnicity, and risk of coronary heart disease. Am J Epidemiol 
1980;111:407-414. 

5. Igra A, Stavig GR, Leonard AR, with special contributions by 
Gamber W, Hawthorne A, Jang VL, Ransom B. Hypertension and 
Related Health Problems in California. Results from the 1979 
California Hypertension Survey. Hyertension Clearinghouse. 
Department of Health Services. Hypertension Control Program. 
714 P. Street. Sacramento, California 95814. 

6. U.S. DHEW. California Conference on High Blood Pressure 
Control in the Spanish-Speaking Community. Summary Report. 
Conference date April 1-2, 1978. NIH Publication No. 
79-1959. August 1979. 

7. Christensen BL, Stallones RA, Insull W, Gotto AM, Taunton 
D. Cardiovascular risk factors in a tri-ethnic population. 
Houston, Texas 1972-1975. J Chron Dis 1981;34:105-118. 

8. Stern MP, Gaskill SP, Allen CR, Garza V, Gonzales JL, Waldrop 
RH. Cardiovascular risk factors in Mexican Americans in 
Laredo, Texas. II. Prevalence and Control of Hypertension. 
Am J Epidemiol 1981;113:556-562. 

9. Apostolides AY, Cutter G, Kraus JF, Oberman A, Blaszkowski T, 
Borhani NO, Entwisle G. Impact of hypertension information 
on high blood pressure control between 1973 and 1978. 
Hypertension 1980;2:708-713. 

10. Fortmann SP, Williams PT, Hulley SB, Maccoby N, Farquhar 

JV. Does dietary health education reach only the privileged. 
The Stanford Three Community Study. Circ 1982;66:77-82. 

11. Stern MP, Gaskill SP, Allen CR, Garza V, Gonzales JL, Waldrop RH. 
Cardiovascular risk factors in Mexican Americans in Laredo, 
Texas. I. Prevalence of overweight and diabetes and distribution 
of serum lipids. Am J Epidemiol 1981;113:546-555. 



408 



12. The Lipid Research Clinics Program Epidemiology Committee. 
Plasma lipid distribution in selected North American 
Populations: Lipid Research Clinics program prevalence study. 
Circulation 1979;60:427-439. 

13. Stern MP, Rosenthal M, Haffner SM, Hazuda HP, Franco LJ. 
Sex differences in the effects of sociocultural status on " 
diabetes and cardiovascular risk factors in Mexican Americans. 
Am J Epidemiol 1984;120:834-851. 

14. Samet JM, Schrag SD, Howard CA, Key CR, Pathak DR. Respiratory 
disease in a New Mexico population sample of Hispanic and 
Non-Hispanic whites. Am Rev Respir Dis 1982;125:152-157. 

15. National Center for Health Statistics. Health Practices 
Among Adults. United States, 1977, by Schoenborn CA, Danchik 
KM. Advancedata. No 64, November 4, 1980. 

16. Roberts RE, Lee ES. Health Practices among Mexican Americans. 
Further evidence from the human population laboratory studies. 
Prev Med 1980;9:675-688. 

17. Rosenwaike I, Preston SH. Age overstatement and Puerto Rican 
longevity. Human Biology 1984;56:503-525. 

18. Gordon T, Garcia-Palmieri MR, Kagan A, Kannel WB, Schiffman 
J. Differences in coronary heart disease in Framingham, 
Honolulu, and Puerto Rico. J Chron Dis 1974;17:329-344. 

19. Gordon T, Kagan A, Garcia-Palmieri M, Kannel WB, Zukel WJ, 
Tillotson J, Sorlie P, Hjortland M. Diet and its relation 
to coronary heart disease and death in three populations. 
Circ 1981;63:500-515. 

20. Sorlie PD, Garcia-Palmieri MR, Costas R, Cruz-Vidal M, Havlik 

R. Cigarette Smoking and Coronary Heart Diseaes in Puerto Rico. 
Prev Med 1982; 11: 304-316^. 

21. Frerichs RR, Chapman JM, Maes EF. Mortality due to all causes 
and to cardiovascular disease among seven race-ethnic populations 
in Los Angeles, County 198a. Int J Epidemiol 1984;13:291-298. 



409 



6.0 SUPPLEMENTARY REFERENCES 

Ramirez EA, Garcia-Pont PH. Relationship of serum cholesterol 
to socioeconomic and dietary factors in Puerto Rican veterans. 
Dis Chest 1969;55:197-201. 

Garcia-Palmieri MR, Tillotson J, Cordero E, Costas R, Sorlie 

P, Gordon T, Kannel WB, Colon AA. Nutrient intake and serum 
lipids in urban and rural Puerto Rican men. Am J Clin Nutr 
1977;30:2092-2100. 

Garcia-Palmieri MR, Sorlie P, Tillotson J, Costas R, Cordero 
E, Rodriguez M. Relationship of dietary intake to subsequent 
coronary heart disease incidence. The Puerto Rico Heart 
Health Program. Am J Clin Nutr 1980;33:1818-1827. 

Costas R, Garcia-Palmieri MR, Sorlie P, Hertzmark E. Coronary 
heart disease risk factors in men with light and dark skin 
in Puerto Rico. Am J Pub Health 1981;71:614-619. 

Health of Minorities and Women. Chartbook. American Public 
Health Association. 1015 Fifteenth Street, N.W. Washington, 
D.C. August 1982. Stock No. 072. 

Health of the Disadvantaged. Chartbook II. DHHS Publication 
No. (HRA)80-633. September 1980. 

Frerichs RR, Chapman JM, Nourjah P, Maes M. Cardiovascular 
Diseases in Los Angeles. 1979-1981. Hansen VE, Ed. American 
Heart Association. Greater Los Angeles Affiliate, Inc. 
1984 edition. 

Chapman JM, Frerichs RR, Maes EF. Cardiovascular Diseases 
in Los Angeles. 1980. Hansen VE, Ed. American Heart 
Association. Greater Los Angeles Affiliate, Inc. 1983 edition. 

U.S. DHHS. Hispanic Health Services Research. NCHSR Research 
Proceedings Series. Conference held September 5-7, 1979. 
DHHS Publication No. (PHS) 80-3288. 

Hayes-Bautista DE . Identifying "Hispanic" populations. 
The influence of research methdology upon public policy. 
Am J Pub Health 1980;70:353-356. 

Roberts RE, Lee ES . The health of Mexican Americans. Evidence 
from human population laboratory studies. Am J Pub Health 
1980;70:375-384. 

Benson H, Costas R, Garcia-Palmieri MR, Feliberti M, Aixala 
R, Blanton JH, Colon AA. Coronary heart disease risk factors. 
A comparison of two Puerto Rican populations. Am J Pub 
Health 1966;56:1057-1060. 



410 



Costas R, Garcia-Palmieri MR, Nazario E, Sorlie PD. Relation 
of lipids, weight, and physical activity to incidence of 
coronary heart disease. The Puerto Rico Heart Study. Am 
J Cardiol 1978;42:653-658. 

Garcia-Palmieri MR, Costas R, Schiffman J, Colon AA, Torres 
R, Nazario E. Interrelationships of serum lipids with relative 
weight, blood glucose, and physical activity. Circ 
1972;45:829-836. 

Garcia-Palmieri MR. Precursors of coronary artery disease 
in Puerto Rico. Am J Clin Nutr 1973;26:1133-1137. 

Garcia-Palmieri MR, Sorlie P, Tillotson J, Costas R, Cordero 
E, Rodriguez M. Relationship of dietary intake to subsequent 
coronary heart disease incidence. The Puerto Rico Heart 
Health Program. Am J Clin Nutr 1980;33:1818-1827. 

Caetano R. Drinking patterns and alcohol problems among 
Hispanics in the U.S. A Review. Drug and Alcohol Dependence 
1983;12:37-59. 

National Center for Health Statistics. Blood Pressure 
Levels of Persons 6-74 years. United States 1971-1974, 
By Roberts J and K Maurer. Vital and Health Statistics, 
Series 11, No. 203. DHEW Publication No. (HRA) 78-1648. 

Caetano R. Self-reported intoxication among Hispanics 
in Northern California. J Stud Alcohol 1984;45:349-354. 

Gordon AJ. The cultural context of drinking and indigenous 
therapy for alcohol problems in three migrant Hispanic 
cultures. J Stud Alcohol 1981 ; (Supp)9 : 217-240. 

Ross CE, Mirowsky J. Social epidemiology of overweight. A 
substantive and methodological investigation. J Health Soc 
Behavior 1983;24:288-298. 

Stern MP, Gaskill SP, Hazuda H, Gardner LI, Haffner SM. 
Does obesity explain excess prevalence of diabetes among 
Mexian Americans? Results of the San Antonio Heart Study. 
Diabetologia 1983;24:272-277. 

Ailinger RL. Hypertension knowledge in a Hispanic community. 
Nurs Res 1982;31:207-210. 

Hazuda HP, Stern MP, Gaskill SP, Haffner SM, Gardner LI. 
Ethnic differences in health knowledge and behaviors related 
to the prevention and treatment of coronary heart disease. 
Am J Epidemiol 1983;117:717-728. 



411 



Nader PR, Baranowski T, Vanderpool NA, Dunn K, Dworkin 
E, Ray L. The Family Health Project. Cardiovascular risk 
reduction education for children and parents. Develop 
and Behavioral Pediatrics 1983;4:3-10. 

Stern MP, Pugh JA, Gaskill SP, Hazuda HP. 

Knowledge, attitudes, and behavior related to obesity and 
dieting in Mexican Americans and Anglos. The San Antonio 
Heart Study. Am J Epidemiol 1982;115:917-928. 

Ramirez AG, Herrick AG, Herrick KL, Weaver FJ. El asesino 
silencioso. A methodology for alerting the Spanish-Speaking 
community. Urban Health 1981;10:44-48. 

Weaver FR, Herrick KL, Ramirez AG, Deatrick DA. Establishing 
a community data base for cardiovascular health education 
programs. Health Values 1978;2:249-256. 

U.S. DHHS. Proceedings of the Conference on Communicating 
with Mexican Americans. Por Su Buena Salud. (Comunicando 
Con Mexico Americanos. For Their Good Health. Conference 
dates September 13-14, 1979. Moore TJ, Ramirez AG, Slayton 
PL, eds. NIH Publication No. 81-1961. June 1981. 



412 



Ischemic Heart Disease 
Risk Factors in Asian/ 
Pacific Islander Americans 




i 



Shiriki K. Kumanyika, Ph.D., M.P.H. 

Department of Epidemiology 

Johns Hopkins School of Hygiene and Public Health 

Baltimore, Maryland 

Daniel D. Savage, M.D., Ph.D. 

Medical Advisor 

National Center for Health Statistics 

Hyattsville, Maryland 



TABLE OF CONTENTS 

1.0 INTRODUCTION 416 

1 . 1 Data Sources 

1 . 2 Approach 

2.0 ISCHEMIC HEART DISEASE MORTALITY AMONG ASIAN/PACIFIC ISLANDERS: 

Trends and Geographic Comparisons 417 

3.0 ISCHEMIC HEART DISEASE RISK FACTORS AMONG ASIAN/PACIFIC ISLANDERS . 419 

3.1 Japanese Americans 

3.1.1 Blood Pressure 

3.1.2 Blood Cholesterol 

3.1.3 Smoking 

3.1.4 Overall Impact of Risk Factors on Ischemic Heart Disease in 

Japanese Americans 

3.1.5 Summary 

3.2 Chinese Americans 

3.3 Filipino Americans 

3.3.1 Blood Pressure 

3.3.2 Smoking 

3.4 Other Asian/Pacific Islanders 

4.0 CONCLUSION 436 

5.0 REFERENCES 437 



415 



1.0 INTRODUCTION 

1.1 Data Sources 

The census definition of Asian/Pacific Islanders refers to a set of 
ethnically and culturally diverse U.S. population subgroups whose origins 
were in the "Far East, Southeast Asia, or the Pacific Islands" (1). 
Relatively recent (1980 or later publication date) ischemic heart disease 
(IHD) or IHD risk studies on Asian/Pacific Islanders identified through the 
Medline search related almost exclusively to Japanese Americans --drawing 
primarily on the Ni-Hon-San Study comparisons of Japanese in Hawaii, 
California, and Japan (2-7) and on the prospective study of the Honolulu 
cohort of Japanese (Honolulu Heart Study) (8-20) . 

Papers on heart disease mortality in Hawaii and Los Angeles compare 
mortality rates of several groups (the Hawaii paper includes data for 
Hawaiian, Filipino, Japanese, and Caucasian men and women (8); the Los 
Angeles County paper includes data for Japanese, whites, Filipinos, 
Chinese, and Koreans (21)). A review of disease trends in Pacific Basin 
countries (22) includes an overview of CHD mortality trends in Japan, 
China, Hawaii, and the Philippines. A California statewide hypertension 
survey presents cardiovascular risk factor data (except lipids) for white, 
Japanese, Filipino, Chinese, and other Asian/Pacific Islander men and women 
(23,24). 

Even recognizing the relatively small amount of data available on 
Asian/Pacific Islander subgroups other than Japanese Americans, the' low 
yield of studies of other Asian/Pacific Islander subgroups from the 
computerized literature search suggests that the NLM searching protocol for 
minorities (i.e. MEDLINE heading: "minorities') may need expanding to 
ensure that Filipinos, Hawaiians, Koreans, and other Asian sub-groups (e.g., 
Vietnamese) are included. Several informative papers on Chinese, 
Filipino-, and Hawaiian-Americans (25-36) were identified 

through ad hoc methods, using the bibliograpy of a recent paper on diabetes 
mortality among New York City Chinese (Current Contents citation) as the 
index paper. 

1 . 2 Approach 

An attempt is made to summarize available data on levels and trends of 
IHD risk factors among Asian/Pacific Islander subgroups in the United 
States. Patterns of IHD or heart disease mortality and incidence are 
presented to provide a perspective in considering the related risk factors 
(and to some extent as a substitute for risk factor data to give at least a 
general impression of patterns in various sub-groups). Available 
information on risk factor levels, trends, and impact in the Asian/Pacific 
Islander population is then presented by risk factor separately for 
Japanese, Chinese, and Filipinos. Where possible, comparisons with levels 
in the U.S. total population or the white population are made. Comparisons 
between or among Asian/Pacific Islander subgroups are noted where they 
appear to give insight into differential effects of migration and 
adaptation among Asian/Pacific Islanders of different origins. 



416 



2.0 ISCHEMIC HEART DISEASE MORTALITY AMONG ASIAN/PACIFIC ISLANDERS: 
Trends and Geographic Comparisons 

A comparison of age-adjusted coronary heart disease (CHD) mortality 
rates among males in the state of Hawaii between 1940 and 1978 (8) 
indicates that rates for Caucasians followed very closely the pattern 
observed for the total population of white men in the U.S. Hawaiian men had 
the highest rates, Caucasian men second highest, Filipino men third, and 
Japanese men lowest. Over the 38 year period between 1940 and 1978, rates 
for Hawaiian and Caucasian men showed almost no net increase--a slight 
upwards slope changed to a downward trend around 1970. Rates for Hawaiian 
men were in the range of 3 per 1000 and for Caucasian men in the range of 2 
per 1000. 

The pattern for Filipino men in Hawaii was quite different from that 
seen in Hawaiian and Caucasian men. CHD mortality among Filipino men 
increased from less than 0.6 per 1000 in 1948 to slightly more than 2 per 
1000 in 1978 with no evidence of the downturn seen in the other three 
ethnic categories. In a detailed analysis of CHD mortality data for 
Filipinos in Hawaii, Gerber noted that CHD mortality rates more than 
doubled during the 20 year period between 1950 to 1970 (1970 rates 2.6 
times 1950 rates), and were significantly related to degree of urbanization 
and to marital status (lowest rates among married males) (27). 

CHD mortality for Chinese in Hawaii was not reported in the paper by 
Reed et al. (8). King reported that 1949-1956 CHD mortality rates for 
Chinese in Hawaii were lower than for Hawaiians or Caucasians but higher 
than for Japanese (28) . More specific data for this period were reported 
by Bennett et al. (29). Age-adjusted death rates for arteriosclerotic 
heart disease including coronary disease (ICD 420) for Polynesian 
(Hawaiian), Chinese, Caucasian, Filipino and Japanese men (ages 35-74 years 
of age, 1949-1956) were 550, 357, 488, 140 and 161/100,000 respectively 
(29). Chinese men had rates lower than Caucasians but considerably higher 
rates than Filipinos and Japanese. Among women, equivalent rates for 
Polynesians, Chinese, Caucasians, Filipinos, and Japanese were 303, 251, 
190, 130, and 94 per 100,000. Thus, Chinese women were at higher risk of 
mortality than women of all ethnicities other than Hawaiian. Data on the 
slope of CHD mortality among Chinese men and women in Hawaii since 1956 
have not been identified at this writing. Gerber and Madhavan reported 
277 CHD deaths among Hawaii Chinese males age 25 or over in 1968-72, but no 
denominator is given for conversion to a rate (30, Table 1). The remaining 
data are presented as proportional mortality. 

CHD mortality rates also increased substantially among Japanese men 
in Hawaii between 1940 and 1978 (less than . 3 in 1940 to about 1.5 in 
1970) but declined somewhat between 1970 and 1978. Patterns for women in 
Hawaii were similar to those of the men in the respective ethnic groups, 
except that rates were lower and downward trends in rates were observed 
among women in all four groups and began in 1960 (rather than 1970) for 
Hawaiian and Filipino women. 



417 



Although the above findings, which were based on Hawaii state death 
certificate data, indicate a decline in CHD mortality for Japanese men from 
the late 1960 's on, no such decline was indicated in data for the Honolulu 
Heart Study cohort (8). In noting this discrepancy, Reed and coworkers 
suggest that the apparent declines indicated in the state mortality records 
may be artifacts of coding changes or misclassif ication of other 
cardiovascular diseases. 

Los Angeles 1980 age-sex adjusted mortality due to heart disease is 
shown in Table 1, below; cerebrovascular disease rates are also shown, for 
comparison. Heart disease mortality is substantially less among 
Asian/Pacific Islanders vs. the white or overall U.S. populations. Among 
Asian/Pacific Islanders, heart disease death rates were highest for 
Japanese, intermediate for Chinese and Korean and lowest for Filipinos. 
The relative mortality ranks for Japanese, Chinese and Filipinos were the 
same for both heart and cerebrovascular disease, although Japanese American 
cerebrovascular disease rates were higher than those for whites or for the 
general U.S. population. 



Table 1. Deaths due to heart and cerebrovascular diseases in 

Los Angeles County, 1980 (from ref 21, Tables 3 and 4) 



MORTALITY: LOS ANGELES COUNTY, 1980 

US White Japanese Filipino Chinese Korean 



# * 



Heart Diseases 
Cerebrovascular Bis 



309 


331 


162 


58 


99 


82 


69 


76 


80 


20 


49 


48 



" rate per 100,000 age adjusted for age and sex by direct method, Los 

Angeles County population 1980 as standard. 
# adjusted for age by direct method, LA county 1980 population as standard. 



Comparison of the adjusted Hawaii and Los Angeles County death rates 
is not appropriate. However, the difference in the relative positions of 
Filipinos and Japanese in Hawaii in 1978 vs. Los Angeles in 1980 is noted. 
In discussing the Los Angeles data, Frerichs et al. (21) suggest that the 
recency of migration of the Chinese, Filipino and Korean populations to the 
Los Angeles area may be responsible for a "healthy migrant" effect on 
mortality rates in these groups. In the same vein, rates for the more 
established Japanese population are closer to those of the Los Angeles 
general population. 

Gerber and Madhavan have compared proportional mortality due to CHD 
among Chinese in Hawaii, native and foreign-born Chinese in New York City, 
and whites in New York City between 1968 and 1972 (30). CHD deaths are 
proportionately higher in Hawaii Chinese vs. New York City Chinese in every 
age-group (for population ages 35 and over) with the size of the difference 



418 



narrowing with increasing age and disappearing in the 75+ age-group. Among 
the Chinese in New York City, CHD deaths were proportionately greater in 
U.S. born vs. foreign-born Chinese at all ages (ages 25 and over). CHD 
mortality represented a lower proportion of deaths among Chinese in both 
Hawaii and New York City vs. whites in New York City, except in the 25-44 
year age-group where proportionate mortality was higher in Hawaiian 
Chinese. Age at CHD death was later in Chinese populations than in New 
York City whites and later in foreign-born New York City Chinese than in 
the other two Chinese subgroups. These findings are consistent with an 
increasing and earlier CHD risk with increasing U.S. exposure. 

These limited data on IHD mortality data for Asian/Pacific Islanders 
indicate generally lower IHD mortality among Asian/Pacific Islander 
subgroups than among United States whites . 

Asian/Pacific Islander women appear to have lower risk than men. The 
subgroup variations in IHD mortality rates and trends among Asian/Pacific 
Islanders are noteworthy and suggest the need to go beyond generalities to 
analyses for each specific subgroup. Subgroup differences are related to 
biocultural factors which are inherently different among groups classified 
as Asian/Pacific Islanders and also to factors such as place of birth 
(native-born or immigrant), age of migration, length of U.S. residence, 
region of residence (e.g., Hawaii, California, New York City), 
socioeconomic status,, and level of acculturation in diet and lifestyle. 
IHD risk appears to increase with increasing length of U.S. residence and 
increasing acculturation. 



3.0 ISCHEMIC HEART DISEASE RISK FACTORS AMONG ASIAN/PACIFIC ISLANDERS 

3.1 Japanese Americans 

3.1.1 Blood Pressure 

[The high rate of stroke and potential effect of stroke mortality among 
Japanese men with elevated blood pressure should be kept in mind when 
considering the data on blood pressure distributions] 

A report by Yano et al. gives mean baseline blood pressure levels in 
45-54 year old men in the Honolulu Heart Study Cohort (1965) as 130.7/82.0 
(systolic/diastolic, mmHg) and the prevalence of elevated blood 
pressure (>160/95) as 16.7% (37). Gordon reported that mean blood pressure 
levels of Honolulu Japanese men 45 to 64 years old (note that age span is 
10 years longer than that cited from Yano et al.; i.e., more older men in 
the Gordon data) were similar to those of men in Framingham (mean SBP 136 
in both groups). Mean diastolic blood pressure levels were somewhat lower 
in the Honolulu men compared to Framingham men (82.68 vs. 85.07) (38). A 
substantially higher prevalence of ECG-LVH in Framingham vs. Honolulu men 
was noted (2.3 vs. 0.7%) in spite of the similarity of blood pressure 
levels. The authors note that the readings were not standardized. 



419 



Comparisons of (1967-1970) systolic blood pressure levels of 
Japanese men living in Japan, Honolulu and California, reported by 
Winkelstein at al . (6), resulted in an overall impression that blood 
pressure levels of home-island Japanese men were intermediate between those 
of Northern California Japanese men, who had the highest levels, and those 
of Hawaii Japanese men. The concluding point of their abstract is that 
"... the blood pressure distributions of the Japanese populations residing 
in Japan, Hawaii, and Northern California cannot of themselves account for 
the observed differences in coronary heart disease and stroke occurrence 
among these populations in which there is a gradient from high stroke rates 
in Japan to low rates in California and a reverse trend for coronary heart 
disease" (6) . 

The specific analyses indicated that Issei Japanese men (men born in 
Japan who migrated to Hawaii or California) under age 55 in all three areas 
have similar blood pressures, but that over the age of 55 California Issei 
men had higher readings than their counterparts in the other two areas. 
Blood pressures of Issei men over age 55 in California were somewhat higher 
than those of the Issei Hawaiian men. 

Diastolic blood pressure levels among Nisei men in California were 
higher than those of the other cohorts at all ages studied. Systolic blood 
pressure levels of both Hawaiian and California Nisei men under age 55 were 
substantially higher than those of the Japanese men in Japan or the Issei 
men in Hawaii and California. Diastolic blood pressures of the men in 
Japan and those of first and second generation Japanese men in Hawaii were 
similar. Systolic blood pressure levels increased with age for all 
cohorts; diastolic blood pressure levels were unrelated to age in the Japan 
and Hawaii cohorts and in the Nisei men in California. Appendix A in the 
Winkelstein et al. paper gives mean blood pressure levels as shown in Table 
2, below (however, most of the analyses presented by Winkelstein et al. are 
based on comparisons of selected percentiles --means are presented here as a 
convention; standard deviations are in the source Table: SDs range from 16 
to 27 for SBP and from 11 to 15 for DBF). 



420 



Table 2. Baseline systolic and diastolic blood pressure levels 

of cohorts of 45-64 year old Japanese men in three geographic regions 

ref.6; Appendix A 





age 


45-49 


50-54 


55-59 


60-64 


65-69 


JAPAN 
















SBP 


126 


130 


136 


140 


143 




DBF 


81 


82 


85 


83 


83 


HAWAII 














Issei 


SBP 


131 


134 


135 


137 


141 




DBP 


80 


86 


82 


80 


81 


Nisei 


SBP 


128 


132 


134 


139 


141 




DBP 


82 


82 


83 


83 


81 


CALIFORNIA 












Issei 


SBP 


123 


132 


139 


146 


148 




DBP 


79 


84 


88 


89 


89 


Nisei 


SBP 


133 


137 


142 


142 


146 




DBP 


88 


89 


90 


89 


90 



The differences in blood pressure levels among these cohorts were 
primarily explained by weight. Weight-blood pressure relationships were 
unstable in the men in Japan; weight and blood pressure were postively 
associated in the other cohorts and adjustment for relative weight 
decreased the blood pressure differences between cohorts. Blood pressure 
levels of the California cohort remained somewhat higher than those of the 
other two cohorts in most of the comparisons . 

Mean blood pressure levels among Japanese men in California in 1979 
were estimated from the California Hypertension Survey data, based on a 
multistage probability sample of the state population, with oversampling in 
primarily Asian American communities (24). The authors of this paper noted 
that in the 1980 census, the Asian/Pacific Islander population of 
California comprised 35.8% of the Asians and Pacific Islanders in the United 
States . 

The California Hypertension Survey (24) estimate of elevated blood 
pressure prevalence (>140/90) among California Japanese men ages 18-49 was 
slightly higher than for white men (19.2 vs. 15.0 %). For men over age 50, 
the prevalence of elevated blood pressure among Japanese men by this 
criterion was lower than for white men (29.1 vs. 38.5 %). Hypertension 
prevalence (140/90) for Japanese women was much lower than for white women 



421 



at all ages: 0.4% vs. 4.8% among Japanese vs. white women ages 18-49 and 
13.9 vs. 36.4% for Japanese vs. white women over age 50. (See Table 9 in 
section 3.4 for 160/95+ prevalence comparisons with sexes pooled.) 

The sex differences in hypertension prevalence among Asian/Pacific 
Islander men and women were reduced 5% by adjustment for age and relative 
weight and further by adjustment for alcohol intake and other environmental 
variables. Rates for the men were only 2.3% higher than those of women 
after adjustment for all significant predictors available (these included 
psychological, social support, nutrition, smoking, and acculturation 
factors) . 

In a more detailed report of the survey results, the prevalence of 
hypertension (i.e., rather than elevated bp) (>140/90 or taking medication) 
among Japanese men and women was as follows (from Table 4.3 in Reference 
23): 

Japanese American men 18-49: 19.8% (vs. 19.2% with bp > or =140/90) 

50+: 32.3% (vs. 29.1% with bp > or =140/90) 
Japanese American women 18-49: 0.9% (vs. 0.4 % with bp > or =140/90) 

50+: 17.5% (vs. 13.9% with bp > or =140/90) 

The parenthetical data are repeated here to indicate the relative 
percents of the populations who are hypertensive under control vs. those 
whose blood pressures were elevated at time surveyed, using the 140/90+ 
definition. 

In the California Hypertension Survey (23) , levels of hypertension 
awareness, treatment and control differed depending on the definition of 
hypertension used. In almost all instances higher percentages of 
awareness, treatment and control were reported for the groups defined by 
the more severe criteria (i.e., 160/95+ or 95+). (This also applies to the 
whites, blacks, and the other Asian/Pacific Islander subgroups surveyed.) 
Awareness among hypertensive Japanese adults ages 50 and older was 72% 
(using 140/90 mm Hg) and 94% (using a diastolic blood pressure of 95 or 
greater mm Hg) in men (60 to 87% in white men) and 60 to 87% in women 
(white women, 70 and 93%) . Awareness levels among Japanese males 18-49 
were 35 to 30% (i.e., 35% aware using 140/90 and 30% aware using 95+ mm Hg, 
a reversed trend) ; (white males 42 to 62%) . 

Percentage of hypertensives under drug treatment were as follows: 12 
to 29% for Japanese men 18-49 (white men 15-38%); (no stable estimates for 
Japanese women ages 18-49) ;37 to 61% for males ages 50 and over (white 
males 40-75%) and 32 to 79% for women ages 50 and over (white women 
52-87%) . Percentages of hypertensives controlled were 3 to 29% for 
Japanese men 18-49 (7-32% for white men) and 10-56% for men 50 and over 
(15-58% for white men). Eight to 38% of Japanese women ages 50 and over 
were controlled (21-78% of white women). 



422 



3.1.2 Blood Cholesterol 

Yano et al. report a mean level of baseline serum cholesterol in the 
younger segment of the Honolulu cohort (ages 45-54) as 219.4 mg% and a 
13.4% prevalence of hypercholesterolemia (>=260 mg%) (37). Comparisons of 
total cholesterol levels in 45-64 year old Japanese men in the Honolulu 
cohort with levels of Framingham men were reported by Gordon et al. in 1974 
(38) . Methodologies for cholesterol determinations were sufficiently 
similar for Honolulu and Framingham to support direct comparisons. Serum 
cholesterol levels were approximately 15% lower in Honolulu vs. Framingham 
(218.55 vs. 233.96 mg%) . 

Baseline comparisons of serum cholesterol levels in Honolulu, Japan, 
and California were reported by Nichaman et al. (4). The essence of the 
overall findings was that in every age-group, mean, median and percentiles 
for each of the biochemical variables are considerably lower for men in 
Japan than in California or Hawaii. . . at all ages the cholesterol 
values in Hawaii are somewhat lower than in California" (4, p. 494) (the 
other biochemical variables examined were glucose, uric acid, and 
triglycerides). Mean levels for the three cohorts are shown in Table 3, 
below. 



Table 3. Mean serum cholesterol levels at baseline (1967-1970) 
for Japanese men in Japan, Hawaii, and California (from ref 
4, Table 3; mg%)-"^ 



AGE JAPAN 



45-49 


179.8 


50-54 


182.5 


55-59 


181.5 


60-64 


182.2 


65-69 


180.9 



AWAII 


CALIFORNIA 


219.4 


223.4 


219.4 


228.2 


218.7 


226.8 


216.7 


223.6 


211.1 


224.0 



" a footnote to the source table notes that the values from Japan 

were taken from the 1967 cycle and that diabetics were excluded 
from this analysis--therefore other published values may differ 
slightly. 

Serum cholesterol levels of a sample of men from the Honolulu and San 
Francisco cohorts were among those analyzed in the Cooperative Lipoprotein 
Phenotyping Study (9). White comparison groups were from Albany NY, Evans 
County GA and Framingham. Mean HDL levels reported in Table 1 of that 
paper are shown in Table 4, below. 



423 



48.7 


49.6 


51.4 


44.8 


45.5 


45.5 


48.3 


48.1 


50.9 


59.0 


56.3 


51.0 


45.9 


48.8 


49.7 


44.0 


46.0 


46.6 



Table 4. Mean HDL-cholesterol level in samples of white, Japanese, 

and black men over age 50 by age-group (ref 9, Table 1) J 

GROUP AGE 

50-59 60-69 70+ 

Albany (white) 
Framingham ((white) 
Evans County (white) 
Evans County (black) 
San Francisco (Japanese) 
Honolulu (Japanese) 



The focus of the Cooperative Lipoprotein Phenotyping analysis was the 
relationship of lipoproteins to CHD. Total cholesterol levels and HDL-C to 
total-C ratios were not reported as such. This limits the ability to 
directly evaluate the data in Table 4. However, considering the 
earlier-cited data indicating similar total cholesterol levels among 
Framingham and Honolulu men and higher total cholesterol levels in San 
Francisco vs. Honolulu men, the data in Table 4, above, do not suggest any 
large difference in proportionate HDL- levels of Japanese American men - 
compared to white men in the same age range. 

3.1.3 Smoking 

The prevalence of cigarette smoking in the Honolulu cohort men ages 
45-54 was reported by Yano et al . (37) as 46.4%. The percent of men 
smoking a pack of cigarettes per day or less was 27.2; 19.2 smoked more 
than one pack per day (37) . In the comparison of 45-64 year old Framingham 
and Honolulu men reported by Gordon et al. (38), 44.1% of Honolulu men vs. 
57.7% of Framingham men were smokers; Honolulu men smoked 10.52 cigarettes 
on average, vs. a 12.26 average among Framingham men. Robertson et al. (5) 
reported the following frequency distributions of baseline smoking status 
for home-island and Honolulu Japanese men ages 45-68 years (ref. 5; Fig. 1) : 

none- <11 11-20 21+ 

Japan 24.4 7.9 56.1 11.6 

Honolulu 55.8 2.5 25.1 16.6 

( " includes former smokers ) 

Taken together, these data indicate that Japanese men in Honolulu were less 
often smokers than Japanese men in Japan and white men in Framingham. 

Marmot and Syme discuss smoking habits in relation to acculturation 
of Japanese men in San Francisco (3) . The data are based on a survey 
conducted in 1969-70 (response rate 66% of the men enumerated in San 



424 



Francisco and Oakland plus additional men in Santa Clara County) . The 
study included 14.6% Issei men. The rest were Nisei (including some Sansei 
(third generation)) men ages 30 and over. Issei men were the older men in 
the cohort . 

Defining traditional vs. nontraditional upbringing according to years 
spent in Japan, age left parents' home, ever lived on a farm, where 
schooling took place (Japan or U.S.), years spent in Japanese language 
school, religion while growing up, friends while growing up, wife's 
cultural background (if married) (3; pp. 230-231) --the following data were 
reported (3; p. 232): 

% of smokers who smoke: 
1-14 15-24 25+ 
cigarettes per day 
traditional 20.7 50.5 28.8 
nontraditional 20.0 50.6 29.4 

Thus, although there may be differences in the percentages of traditional 
and nontraditional men who smoke, there are no differences in level of 
smoking among those who do smoke. Also, the authors note a possible 
interaction between Japanese vs. Western diet preference and smoking among 
the men surveyed- -there was a somewhat higher percent of smokers among men 
who preferred a Japanese diet. 

More recent estimates of cigarette use among Japanese Americans in 
California are available from the 1979 survey results. Overall, 50.6% of 
the Japanese American men were classified as "ever smoked" (24). A more 
detailed breakdown of smoking habits in this population is shown in Table 
5, below. 



Table 5. Cigarette Smoking Variables among Japanese American men and women 
in the California Hypertension Survey, 1979 (from reference 23, Table 7.5) 
[percentages for comparable white sex-age-group] 



%current regular smokers 



%current or former smokers 



average cigarettes smoked per 
day among current smokers 

%of current smokers who 
would like to quit 

"=based on fewer than 20 cases 



Men 


Men 


Women 


Women 


18-49 


50+ 


18-49 


50+ 


34.8 


17.7 


19.0 


18.1 


[ 34.6 


30.5 


36.5 


25.9 ] 


55.0 


81.1 


47.4 


29.5 


[ 58.0 


72.6 


52.2 


48.7 ] 


19.3 


19.9 


17.6 


11.7 


[ 26.5 


28.3 


23.4 


23.2 ] 


80.4 


40.2 


56.1 


5.9* 


[ 71.0 


59.0 


63.8 


60.8 ] 



425 



3.1.4 Overall Impact of Risk Factors on CHD in Japanese Americans 

Earlier, the discrepancy between Hawaii state mortality data and 
Honolulu Heart Study findings regarding CHD mortality was noted. The 
Honolulu data did not show declines in CHD mortality in analysis of data 
for 60 to 69 year old men between 1968 and 1978 using causes coded from 
medical records review, whereas the data coded according to state mortality 
codes did show a decline (see Reed et al. (8, Figures 3 and 6)). 

Reed et al. present total and fatal myocardial infarction (MI) 
incidence data for 50-59, 60-63, and 64-67 year old men in this cohort in 
Figure 4 of their report. Incidence rates for total MI increased overall 
between 1967-70 and 1975-78 for men ages 60-67 and appear to have remained 
constant in the 56-59 year old men. Fatal MI rates showed a slight 
increase in the 60-67 year old men with evidence of tapering off after 
1971-74; fatal MI rates were constant in the 56-59 year old men. 
Case-fatality rates for the three age groups are presented in Table 1 of 
the report: 37, 39, and 36% in men 56-59 during the three time periods; 
36, 42, and 33% in 60-63 year old men; and 46, 45, 45 percent in men ages 
64-67. Analyses by birth cohort indicate upward slopes of total and fatal 
MI incidence during this time period in all cohorts of men born between 
1900 and 1919. 

Gordon et al. (38) reported that although the standard risk factor 
associations were observed among men in the Honolulu cohort, the 2 year CHD 
incidence (by ECG) or mortality in Honolulu was less than in Framingham by 
one-half to one fourth. Incidence was 2 times more in Framingham and 
mortality was 4 times more i.e., the case-fatality in Honolulu was much 
lower than in Framingham. CHD mortality in Framingham was greater by a 
factor of 2.1 even after adjustment for differences in levels of blood 
pressure, smoking, and cholesterol (this finding was not substantially 
changed by exclusion of men with prior CHD from the analysis) . Castelli et 
al. point out that Honolulu men have CHD incidence half that of Framingham 
men in spite of the fact that HDL cholesterol levels of the two groups of 
men are similar (9). Framingham CHD rates were higher than Honolulu rates 
even in the group with low risk factor levels. Differences in Framingham 
and Honolulu rates increased in magnitude with increasing age. 

In a later analysis of six year follow-up data (10) Gordon et al. 
attempted to identify factors other than blood pressure, smoking and 
cholesterol which could explain the differences between Framingham and 
Honolulu CHD rates. Alcohol intake was found to be a strong inverse 
predictor of MI and CHD death although the authors noted that total 
mortality was increased with increased alcohol consumption (possibly 
positive effect of alcohol on blood pressure and/or stroke) . Higher starch 
intake in the Honolulu cohort was also noted as a significant protective 
factor for CHD. Elsewhere, the possible differential factor of later age 
of acquisition of risk factors among Japanese migrants vs. U.S. -born men 
has been noted as a possible explanation for CHD rates less than those 
predicted with Framingham logistic functions (5). 



426 



Robertson compared risk factor-CHD associations in Japanese men in 
Honolulu and Japan (5). Gradients for blood pressure and cholesterol on 
CHD incidence were similar in both cohorts of men. Smoking was the most 
significant risk factor in Honolulu but was not related to CHD incidence in 
Japan (suggesting to the authors that cigarette smoking may be a less 
important CHD risk factor in men with low serum cholesterol levels) . An 
influence of relative weight on CHD was observed in Honolulu Japanese men 
but not among the men in Japan (this finding may have been due to the 
relatively small number of obese men in the Japan cohort (authors' note)). 

In spite of higher blood pressure levels in the California cohort, as 
reported by Winkelstein et al. (6), the authors note that a separate study 
of CHD prevalence in the three cohorts did not find a higher CHD prevalence 
among the California men (there are several possible explanations for this 
other than the lack of a true relationship). However, the Honolulu Heart 
Study prospective data found a substantial impact of blood pressure on CHD 
at ten-year follow-up (and throughout) (37) . 

In the ten-year Honolulu Study data, the significance of blood 
pressure levels for total, fatal, and nonfatal CHD, nonfatal MI and acute 
coronary insufficiency compared with nonCHD was great. In fact, systolic 
(or diastolic) blood pressure was one of the strongest and most 
consistently related risk factors of those measured, for all CHD measures 
except angina pectoris (see Table 6, below). 



Table 6. Impact of standard risk factors, body mass index and 
alcohol intake on CHD among Japanese American men in Honolulu 
at ten-year follow-up (from 37, Table 2 (age-adjusted means 
for baseline characteristics) 



SBP 



DBF 



CHOL'^ 



CIGS# 



BMI-' 



ALCH! 



nonCHD 


133.2 


81.9 


217.0 


10.2 


23.8 


14.3 


Total CHD 


144.7 


86.6 


229.9 


13.0 


24.7 


9.7 


Fatal CHD 


151.6 


89.0 


231.3 


14.2 


24.8 


9.1 


nonfatal, MI 


143.2 


86.0 


223.0 


14.6 


24.8 


8.3 


Acute CI 


147.1 


87.4 


222.7 


14.2 


24.8 


15.6 


uncomp AP 


137.2 


84.0 


,225.4 


7.3 


24.5 


10.5 



serum chol mg/o;y/no. per day;"" kg/m squared; !ml/day 



Levels of these variables were significantly different from the nonCHD 
group for the total CHD cases, for fatal CHD cases (except alcohol 
consumption), and for nonfatal MI. Acute coronary insufficiency cases 
differed from the nonCHD only for blood pressure (the authors note that 
less than valid ascertainment of angina pectoris may be involved in the 
apparent lack of associations with this CHD manifestation) . 



427 



Multivariate analyses (see 31, Table 4) indicated that, in addition to 
blood pressure, cigarette smoking was next in line as a strong predictor of 
CHD in all categories except angina. Alcohol consumption was a strong, 
independently associated protective factor for both fatal CHD and for 
nonfatal MI. Serum cholesterol was strongly associated with total CHD and 
nonfatal MI and significantly, but less strongly related to fatal CHD. 
Relative weight was not independently associated with any of the CHD 
manifestations in the multivariate analysis. 

3.1.5 Summary 

These data, although far from adequate in describing the overall IHD 
risk patterns among Japanese American men and women, can be summarized as 
follows . 

Systolic blood pressure levels of Japanese men in the Honolulu Heart 
Study cohort were similar to those of Framingham men; diastolic blood 
pressures were somewhat lower. The EKG-LVH prevalence among the Japanese 
men was lower than expected based on the Framingham model, possibly related 
to methodology. A consistent gradient in blood pressure and blood pressure 
related risk is not evident when comparing Japanese men in Japan, Hawaii, 
and California. U.S. born Japanese men in California have higher blood 
pressure levels than men in Japan or Japanese-born men in California; these 
differences appear to be weight-related. 

When compared to white men in California, Japanese men under age 50 
had a hypertension prevalence slightly higher than that of white men 
whereas Japanese men above 50 had a lower hypertension prevalence than 
white men. Hypertension awareness was somewhat higher among Japanese men 
over age 50 compared to white men in that age-group but was lower among 
Japanese men under age 50 compared to white men. Percentages of Japanese 
men under drug treatment were somewhat lower than for white men. 
Percentages of those treated who were controlled were similar among 
Japanese men and white men. 

Japanese women in California had substantially lower hypertension 
prevalence than white women in both the under 50 and 50 and over age 
groups . Weight and other environmental factors would appear to explain 
most of the gender differences in hypertension prevalence. Small numbers 
precluded estimates of hypertension awareness, treatment, and control among 
Japanese women under age 50. Data for hypertensive women over age 50 
indicated lower levels of awareness, treatment, and control compared to 
white women in this age-group. 

The limited available data on serum cholesterol levels of Japanese men 
indicate a consistent gradient in serum cholesterol levels from low levels 
among Japanese men in Japan to intermediate levels among Japanese men in 
Hawaii and the highest levels among Japanese men in California. Serum 
cholesterol levels of Japanese men in all three areas were lower than for 
men in Framingham. No data on cholesterol levels of Japanese American 
women were identified. 



I 



428 



Regarding smoking, the prospective study baseline data suggest that 
Japanese men in Hawaii were less likely to be smokers than men in Japan or 
Framingham. The more recent California survey data suggest similar smoking 
rates among Japanese and white men under age 50, but lower smoking rates 
among the older Japanese men compared to older white men. Smoking rates 
among Japanese women respondents in the California survey were lower than 
for white women, in both the younger and older age-groups. The average 
number of cigarettes smoked by Japanese men and women was consistently less 
than for the comparable white age-sex group. Somewhat more of the younger 
Japanese men wanted to quit smoking compared to the white men in the same 
age-group; otherwise, the Japanese surveyed were less likely than their 
white counterparts to state that they wanted to stop smoking. 

The impact of the standard risk factors on IHD morbidity and 
mortality, although less than predicted at short-term prospective 
follow-up, has been in line with expectations upon longer (10-year) 
follow-up. Thus, at least tentatively, these data indicate that Japanese 
Americans have IHD risks comparable to those of white Americans to the 
extent that they acquire comparable risk factor profiles. The lower IHD 
mortality rates among Japanese Americans may reflect somewhat lower levels 
of certain IHD risk factors, particularly among the older Japanese men who 
are primarily Japan-born. 

3.2 Chinese Americans 

Primary findings from the available data sources on risk factors among 
Chinese Americans are summarized in this section. Refer to the earlier 
description of CHD mortality data for Chinese Americans (section 2.0). A 
report by Gerber of higher proportional diabetes mortality among Chinese in 
New York City compared to whites and other nonwhites in New York City 
should be noted as well (31). Among 45-64 year old foreign-born Chinese, the 
proportion of diabetes deaths increased with increased length of residence 
in New York City. Proportional mortality from diabetes was slightly higher 
in foreign born vs. U.S. born Chinese above age 65, but slightly lower 
among foreign-born Chinese ages 45-64. 

A component of the Hawaii Cardiovascular Study compared cardiovascular 
risk factors in 30 Chinese and 68 Japanese males who had Mis with those of 
CHD-free controls in 1966 and 1967 (25). The comparison was prompted by 
the higher risk of CHD in Chinese men- -2. 2 times that of the Japanese men. 
Cases were identified through hospital discharge records. Examinations 
were at least 3 months post-discharge. Controls were age- and race-matched 
men identified through hospital records as well as an additional group of 
population controls randomly selected from a health department survey 
sample. Absence of CHD in controls was electrocardiographically confirmed. 
Racially-mixed Chinese and Japanese men were not included in the study. 
Chinese cases were older than Japanese cases by about 5 years (58.4 vs. 
53.2 years of age). Racial comparisons were therefore age-adjusted. 

Recognizing the inherent possibilities for sample biases among the 
cases, the emphasis of the analyses was in racial rather than case-control 
comparisons. Significant differences between the Chinese and Japanese 



429 



cases which were also seen in the population controls were considered to 
have greater probable validity than differences which were apparent between 
Japanese and Chinese controls only. 

The Chinese men were more obese than the Japanese (skinfolds) and 
appeared to have gained more weight since age 25, but were not more 
overweight by a weight/height index (Quetelet) . In a follow-up report on 
the Chinese MI survivors and controls, these authors confirmed that the 
moderate, "nonoverweight" adiposity among the Chinese men was of 
pathological significance, i.e., it was related to higher levels of 
CHD and CHD risk factors (32). 

Serum cholesterol levels of the Chinese population controls were 
approximately 20 mg% higher than those of the Japanese controls (242.7 vs. 
220.7); higher cholesterol among the Chinese vs. Japanese men was generally 
consistent in age-specific comparisons although not always statistically 
significant. Blood pressure levels and LVH patterns were not consistently 
or significantly different between the two racial groups. A slightly 
higher proportion of Japanese vs. Chinese cases were smokers (75 vs. 70%) 
in the immediate pre-MI period; higher proportions of Chinese patients and 
both groups of controls had never smoked and fewer were current smokers 
than the respective groups of Japanese men. Physical activity was lower in 
the Chinese than Japanese men. 

According to Stavig et al., the Chinese population of California 
increased by a factor of 2.5 between the 1970 and 1980 censuses (24). 
Estimates of elevated blood pressure prevalence (> or =140/90) among California 
Chinese men ages 18-49 was slightly lower than for comparable white men 
(11.8 vs. 15.0%). For Chinese men over age 50 the prevalence of elevated 
blood pressure by this criterion was higher, 45.0 vs. 38.5% for white men. 
Elevated blood pressure prevalence (140/90+) for Chinese women vs. white 
women was similar: slightly higher in the 18-49 year age-group (6.4 vs. 
4.8%) and essentially the same (34.3 vs. 36.4%) for women ages 50 and over 
(also see Table 9, section 3.4). 

The overall influence of age, relative weight and other predictive 
variables on the prevalence of elevated blood pressure among Asian/Pacific 
Islanders in the 1979 California survey was described earlier (section 
3.1.1). Chinese in California were intermediate (between Japanese and 
Filipinos) in reported alcohol intake, the least likely of the three 
sub-groups to be foreign-born, and varied in comparability to the other two 
groups on other blood pressure predictors. 

In the more detailed report of the survey results, the prevalence of 
hypertension (rather than elevated blood pressure) (> or =140/90 or taking 
medication) among Chinese men and women was as follows (from Table 4.3 in 
reference 23) : 

Chinese American men 18-49: 13.3 % (vs. 11.87% with bp > or =140/90) 

50+: 50.3% (vs. 45.0% with bp > or =140/90) 
Chinese American women 18-49: 7.1% (vs. 6.4 % with bp > or =140/90) 

50+: 42.6% (vs. 34.3% with bp > or =140/90) 



430 



The parenthetical data are repeated here to indicate the relative 
percents of the populations who are hypertensive under control vs. those 
whose blood pressures were elevated at time surveyed, using the 140/90+ 
definition. 

Levels of hypertension awareness among hypertensive Chinese ages 50 
and older in California in 1979 were 58 to 83% in men (white men, 60-87%) 
and 55 to 98% in women (white women 70-93%), depending on the definition of 
hypertension used. Awareness levels among Chinese males 18-49 were 32 to 
79% (white men 42-62%) (23, Table 4.4). 

Percentages (of hypertensives) under drug treatment were 21 to 63% for 
Chinese men 18-49 (white men 15-38%); no stable estimates for 
Chinese women aged 18-49; 40 to 68% for males ages 50 and over (white 
males 40-75%); and 52 to 97% for women ages 50 and over (white women, 
52-87%). Percentages of hypertensives under control were 11 to 48% (white 
men 7-32%) for Chinese men 18-49 and 11-59% for men 50 and over (white men 
15-58%). Nineteen to 94% of Chinese women ages 50 and over (white women 
21-78%) were controlled. 

Smoking data for Chinese men and women from the detailed California 
Hypertension report are summarized in Table 7. 



Table 7. Cigarette Smoking Variables among Chinese American 
men and women in the California Hypertension Survey, 1979 (from 
reference 23, Table 7.5) [comparison data for whites] 



Men Men 

18-49 50+ 

% current regular 26.6 35.2 

smokers [34.6 30.5 



% current or 42.0 69.8 

former smokers [58.0 72.6 



average cigarettes 12.5 16.4 

per day among [26.5 28.3 

current smokers 

% of current smokers 54.3 59.0 

who would like to quit [71.0 59.0 

* based on fewer than 20 cases 



Women 


Women 


18-49 


50+ 


3.6 


9.7 


36.5 


25.9 ] 


7.7 


19.2 


52.2 


48.7 ] 


12.0 


17.1 


23.4 


23.2 ] 


48.0* 


66 . 5* 


63.8 


60.8 ] 



431 



In summary, pertinent data which permit interpretation of IHD risk 
factor levels among Chinese American men and women in the context of levels 
of risk typical for the U.S. white population are essentially limited to 
the data from the California survey. The California data indicate higher 
hypertension prevalence among Chinese men over age 50 compared to white 
men, but somewhat lower rates among Chinese men compared to whites in the 
under 50 age-group. Among Chinese and white women in both age-groups the 
rates of hypertension are similar and are lower than for men. 

No serum cholesterol data are available from the California survey. 
The smoking data indicate that more of the older Chinese men, but fewer of 
the younger men, smoke compared to their white age peers. Substantially 
fewer Chinese women smoke than white women in both age-groups. At all 
ages, the Chinese who smoke smoke fewer cigarettes per day. Younger 
Chinese men and women are less likely than their white counterparts to 
report wanting to quit smoking. Older Chinese men and women were equally 
or more likely to report wanting to quit compared to whites. 

Only proportionate mortality data were identified for the Chinese 
population in New York City. These data indicate lower IHD risk among 
Chinese relative to whites, although the proportion of diabetes related 
deaths is higher among Chinese than among whites . 

These data are too limited to support any overall conclusions about 
patterns of IHD risk among Chinese Americans. There does not appear to be 
any striking evidence of excess IHD risk on the basis of these data; most 
of the available data suggest less than average risk among 
Chinese Americans compared to whites. 



3.3 Filipino Americans 

Other than the mortality data for Filipinos reported in section 2.0 
above, the only relevant data identified specific to Filipino Americans was 
from the California Hypertension Survey. Data from that survey for blood 
pressure and smoking are noted below. No serum cholesterol data for 
Filipino Americans have been identified at this writing. 

3.3.1 Blood Pressure 

Mean blood pressure levels among Filipino men in California in 1979 
were estimated from the California Hypertension Survey data (24) . Stavig 
et al. note that the Filipino population of California tripled between 1970 
and 1980. Estimates of elevated blood pressure prevalence (> or =140/90) 
among California Filipino men and women were higher at all ages and 
substantially higher than for whites in the age-sex groups with relatively 
high prevalences: Filipino men 18-49, 29.5% vs. 15.0% for whites; Filpino 
men ages 50+, 50.8% vs. 38.5% for whites; Filipino women 18-49, 6.5% vs. 
4.8% for whites; Filipino women ages 50+, 61.3% vs. 36.4% for whites (24, 
Table 1) (also see Table 9, section 3.4). 



432 



The influence of age, relative weight, and other predictors on blood 
pressure levels of California Asian/Pacific Islanders was noted earlier in 
the discussion of blood pressure levels of Japanese Americans. Filipinos 
and other Asian-Pacific Islanders in California reported a greater 
prevalence of excess weight (higher body mass index) , higher average number 
of alcoholic drinks per sitting, and fewer close friends, were less likely 
to live in Asian neighborhoods and more likely to be foreign born than 
Japanese and Chinese-_consistent with the higher prevalence of uncontrolled 
hypertension in Filipinos vs. Chinese and Japanese. Educational attainment 
was lower among Filipinos, particularly among Filipino men, vs. the general 
population or Japanese American males. 

In the more detailed report of the survey results, the prevalence of 
hypertension (>140/90 or taking medication) among California 
Filipino American men and women was as follows (from Table 4.3, ref. 23): 
Filipino American men 18-49: 30.5% (vs. 29.5% with bp > or =140/90) 

50+: 60.0% (vs. 50.8% with bp > or =140/90) 
Filipino American women 18-49: 6.7% (vs. 6.5 % with bp > or =140/90) 

50+: 65.2% (vs. 61.3% with bp > or =140/90) 

The parenthetical data are repeated here to indicate the relative 
percents of the populations who are hypertensive under control vs. those 
whose blood pressures were elevated at the time surveyed, using the 140/90+ 
definition. 

Levels of hypertension awareness among hypertensive Filipino men and 
women ages 50 and older in California in 1979 were 67 to 91% in men (white 
men 60-87%) and 49 to 83% in women (white women, 70-93%), depending on the 
definition of hypertension used. Awareness levels among Filipino males 
18-49 were 62 to 89% (white males 42-62%) (23, Table 4.4) (stable estimates 
for women 18-49 were not possible) . 

Percentages under drug treatment were: 52 to 82% for Filipino men 
18-49 (white men 15-38%); (no stable estimates for Filipino women aged 
18-49); 43 to 76% for males ages 50 and over (white males 40-75%) and 39 to 
82% for women ages 50 and over (white women 52-87%) . Percentages of 
hypertensives who were contxolled were 3 to 38% for Filipino men ages 18-49 
(white men 7-32%) and 15 to 60% for men ages 50 and over (white men 15-58%). 
Six to 54% of Filipino women ages 50 and over (white women, 21-78%) were 
controlled. 

In summary, an excess prevalence of hypertension among Filipinos in 
California is evident, a noteworthy departure from the picture seen in the 
other Asian/Pacific Islander populations discussed in this review. 
Awareness of hypertension was relatively high, particularly among the 
younger Filipino men compared to white men in the same age-group. 
Percentages of Filipino men under drug treatment and controlled were 
comparable to or better than for white men. Among hypertensive Filipino 
women over age 50, awareness, treatment, and control levels were lower than 
for white women. 



433 



3.3.2 Smoking 

Fewer Filipino than white men and women in the California survey were 
smokers, in both the under 50 and 50 and over age-groups (as shown in Table 
8). Among men and women who smoked, Filipino men and women smoked fewer 
cigarettes per day. The estimates of percentages of Filipino smokers 
wanting to quit are not stable. 



Table 8. Cigarette Smoking Variables among Filipino American 
men and women in the California Hypertension Survey, 1979 (from 
reference 23, Table 7.5) [comparison data for whites] 



% current regular 
smokers 

% current or 
former smokers 

average cigarettes 
per day among 
current smokers 



% of current smokers 

who would like to quit [ 71.0 



Men 


Men 


18-49 


50+ 


30.7 


21.2 


[34.6 


30.5 


58.3 


67.2 


[ 58.0 


72.6 


18.2 


17.2 


[ 26.5 


28.3 


75.6 


90.8^^ 


f 71.0 


59.0 



Women 


Women 


18-49 


50+ 


12.4 


16.1 


36.5 


25.9 ] 


32.9 


25.9 


52.2 


48.7 ] 


15.0 


1.1 


23.4 


23.2 ] 


67.6''^ 


13.2^ 


63.8 


60.8 ] 



" based on fewer than 20 cases 



3.4 Other Asian/Pacific Islanders 



CHD mortality data for Koreans in California are included in Table 1 
(section 2.0). Blood pressure data for "other Asians" in the California 
survey are shown in Table 9, below, with data for Caucasian, Japanese, 
Chinese and Filipinos included for summary and comparison purposes. 



434 



Table 9. 



PERCENT HYPERTENSIVE: CALIFORNIA ADULT (>18 years) 
(from reference 24; Table 1) 



White Japanese Filipino Chinese 



Other 
Asian/ PI 



MALES 18-49 
weighted 
% hypert 
140/90+ 


15.0 


19.2 


29.5 


11.8 


28.5 ^ 


MALES 50+ 
140/90+ 


38.5 


29.1 


50.8 


45.0 


45.2 


FEMALES 18-49 
140/90+ 


4.8 


0.4 


6.5 


6.4 


3.2 


FEMALES 50+ 
140/90+ 


36.4 


13.9 


61.3 


34.3 


42.2 


BOTH SEXES 

18+ 

140/90+ 


20.2 


12.5 


24.5 


15.7 


20.1 


BOTH SEXES 

18+ 

160/95+ 


6.6 


4.3 


9.9 


5.8 


8.2 



The overall rate of hypertension for Asian/Pacific Islanders is 18.9% 
compared to an overall rate of 19.3 for whites. However, this similarity 
in rates is not a true reflection of the heterogeneous picture evident in 
Table 9. The high rates of hypertension among the Filipino men and women, 
the older Chinese men, and the younger Chinese women relative to whites in 
the same sex-age-groups have been noted. Also, hypertension rates are 
higher than those of whites among three of the four sex-age-groups of 
"other" Asian/Pacific Islanders. 



Additional relevant information is sparse but includes more detailed 
data on "other Asians" from the California Survey (23), the Kraus et al. 
analyses of CHD risk factors in several ethnic groups (data are for 
Asian Americans, not further specified) (39), and data for Hawaiians 
(Polynesians) from the Hawaii Cardiovascuar Study (33-36). The paucity of 
data reflects the relatively small numbers of "other Asians" rather than a 
lack of need for concern about significant levels of CHD risk. 



435 



4.0 CONCLUSION 

In conclusion, the data on IHD risk among Asian/Pacific 
Islanders as a group and especially for specific subgroups are 
extremely limited. What data there are indicate that IHD risk 
levels are generally lower than for whites, but with some 
noteworthy exceptions . The extent of IHD risk appears to 
parallel the degree of acculturation. Risks associated with 
diet and lifestyle adaptations to the U.S. environment may be 
important contributors to excess risks as they occur. 



ACKNOWLEDGEMENTS 

We gratefully acknowledge the editorial assistance of Sandra 
J. Anderson and Elisabeth Pitt. 



436 



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441 



Ischemic Heart Disease 
Risk Factors in American 
Indians and Alaska Natives 



Shiriki K. Kumanyika, Ph.D., M.P.H. 

Department of Epidemiology 

Johns Hopkins School of Hygiene and Public Health 

Baltimore, Maryland 

Daniel D. Savage, M.D., Ph.D. 

Medical Advisor 

National Center for Health Statistics 

Hyattsville, Maryland 




TABLE OF CONTENTS 
1.0 APPROACH 446 

2.0 OVERALL PERSPECTIVE ON PREDISPOSITION TO ISCHEMIC HEART 

DISEASE IN NATIVE AMERICANS 447 

2.1 Background Comments on the Native American Population 

2.2 Heart Disease in the Mortality Profile of the Native American 
Population 

3.0 ISCHEMIC HEART DISEASE IN SPECIFIC INDIAN POPULATIONS . . . .453 

3.1 Southwestern Indians 

3.2 Indians outside of the Southwest 

3 . 3 Summary 

4.0 ISCHEMIC HEART DISEASE RISK FACTORS IN NATIVE AMERICANS . . .457 

4.1 General Comments 

4.2 Hypertension 

4.3 Cholesterol 

4.4 Smoking and Alcohol Use 

5.0 MULTIVARIATE PERSPECTIVE 466 

6.0 IMPLICATIONS AND RECOMMENDATIONS ^^^ 

7.0 REFERENCES 469 



445 



1.0 APPROACH 

In general, ischemic heart disease (IHD) risk factor data sources for 
the Native American population are in no sense comparable to those for the 
other minority groups, due to the relatively greater emphasis on health 
problems other than IHD in this population and to the general paucity of 
data specific to the Native American subset of the U.S. non-white 
population. The size of the Native American population is small compared 
to the larger minority of black Americans. Numbers in research reports and 
vital statistics categories relevant to cardiovascular risk are extremely 
small due to the young age of the Native American population and to their 
excess mortality from noncardiovascular causes (1,2). Rates and 
percentages in this report should be interpreted with the small numbers in 
mind. 

The anthropological, socio-political, and cultural history of the 
Native American population is unique and varies greatly among Indian 
tribes. These factors have had a large influence on the amount and nature 
of health and disease data available for this population. Related to this, 
there is considerable redundancy in the authorship of cardiovascular 
studies in Native American populations, a greater than desired reliance on 
inherently biased data sources and anecdotal material, and relatively 
little written about Native American health by Native American people. 

Socioeconomic status of Native Americans is generally at the low end of 
the continuum. Thus, it is difficult to separate genetic and cultural 
factors from socioeconomic factors. Varying degrees of racial admixture 
and inconsistencies in racial classification of Native Americans of mixed 
ancestry (i.e., as Indian vs. white) also complicate the picture of Native 
American-white differences in disease patterns. 

A summary of selected background information on Native American 
population and mortality characteristics has been included, to indicate our 
perspective on IHD risk in this population group (section 2) . Patterns of 
IHD and IHD risk in specific Indian populations are then discussed 
(sections 3 to 6) . 

A large portion of the literature pertinent to cardiovascular risk 
factors relates to Indians in the Southwest and, in particular, to Pima 
Indians, who are reported to have the "highest recorded prevalence of 
diabetes in the world" (50% prevalence in Pima over age 35; almost 
exclusively type 11) (3, page 199). Pima or the closely-related Papago 
Indians are a focus or sub-focus of a third of the papers identified as 
relevant to this report 3,7,12-25). There are also several references 
which provide information on Navajo or Apache Indians 

(3,7,11,22-27,29-31,38). Papers on southwestern Indians include the above 
groups as well as Hopi Indians and other tribes in the Arizona and New 
Mexico area (3,7,22-24,29,30) 

Papers from Minnesota (33,51) provide data primarily on Ojibwa 
(Chippewa) Indians; small percentages of Sioux and Winnebago Indians are 
also represented in the Minnesota Native American population. Other 



446 



relevant studies provide data on aspects of CHD risk among Crow and 
Northern Cheyenne Indians in southeast Montana (34) , Arapaho and Shoshone 
Indians in Wyoming (35), Seminole Indians in Oklahoma and Florida (36), 
Alaska Natives (37,50); j ibwa Indians in Canada (38), Seneca Indians in 
upstate New York (39,40), American Indian university students in Georgia 
(41), and the Tarahumara Indians in Mexico (32,42). 

The literature identified gives a less than complete picture of IHD risk 
for the sub-groups listed above and leaves a substantial portion of the 
Indian population uncovered (4,5). Published tables for the U.S. 
population usually present Native American data in an aggregate "non-white" 
category along with data for black- and/or Hispanic- and/or Asian-Americans 
(9,10). One tabulation of blood pressure levels of nonreservation Indians 
was identified in an NCHS report from the National Health and Nutrition 
Examination Survey, 1971-74 (43). Mortality data for some years were 
obtained from Indian Health Service reports (2,6,8,44) for Indians and 
Alaska Natives in reservation states. 



2.0 OVERALL PERSPECTIVE ON PREDISPOSITION TO ISCHEMIC HEART 

DISEASE IN NATIVE AMERICANS 

2.1 Background Comments on the Native American Population 

The census designation "Native American" includes American Indians, 
Eskimos, and Aleuts. Native Americans were 0.6% of the United States 
population in the 1980 census--l,418,000 of the 226,505 million Americans 
counted (9, Table 1). In the 1970 census, Native Americans were 0.4% of the 
population--793,000 of 203,212,000 Americans counted (10, Table 1). The 
Native American population is disproportionately poor, has a lower 
life expectancy and is younger than the U.S. population as a whole (median 
age 18.4 vs. U.S. population median of 28.1 years in the 1970 census (3,8) 

The Navajo, the largest of several hundred American Indian tribes 
residing in the U.S., numbered approximately 150,000 in the mid-70's (3). 
States with the largest Native American populations are Arizona, Oklahoma, 
California, New Mexico (3), and North Carolina (45) but the federally 
recognized Indian tribes are "spread throughout more than 25 states (3,5). 

Ninety percent of Indians lived on reservations prior to 1940. In 
1970 and 1977, 40% and 51% of Indians lived off of reservations, primarily 
in urban settings (45). Sievers and Fisher (3) point out that southwestern 
Indians have remained more isolated and less racially mixed than Indians in 
other regions. In recent decades however, social and environment changes 
have been occurring, leading to reduced ethnicity. For example, whereas 
60% or more of White Mountain Apaches lived in traditional tribal dwellings 
in 1959, these "wickiups" have become rare. At the time the Sievers and 
Fisher review was written, (1981 publication date) 6% of southwestern 
Indians over age 15 vs. 20% of the population under age 15 were reported to 
have some non- Indian admixture. 



447 



2.2 Heart Disease in the Mortality Profile of the Native American 
Population 

The mortality profile of Native Americans differs from that of the 
overall U.S. population (Tables 1 and 2) and to some extent from that of 
other racial minorities (Table 2) . Age-adjusted total mortality 
comparisons are not given in the 1979 Indian Health Service tables 
available at this writing. Age-adjusted total mortality among Native 
Americans was 1.3 times that for U.S., all races in 19 75 (see Table 3 in 
this report) . 

There were 19,474 deaths among Indians and Alaska Natives in 1979 
(1,913,814 deaths among all races, U.S.). Table 1 indicates that, although 
the majority of deaths are classified as due to heart disease in both the 
general population and among Native Americans, the proportionate mortality 
from heart disease in Native Americans is half that of the general 
population (Note however, that proportionate mortality from heart disease 
varies significantly by region. See Table 5 and accompanying text.) The 
proportion of accidental deaths among Native Americans is nearly as high as 
that due to heart disease and is more than three times as high as the 
proportion of accidental deaths in the general population. The proportion 
of Native American deaths associated with chronic liver disease or 
cirrhosis is 3.8 times higher than in the general population. 



Table 1. Leading causes of death among the U.S., all races 1979 
and comparable data for Indians and Alaska Natives, 
1978-1980 [taken from Table 4.1 in reference 2]. 

Percent Distribution 

Causes of Death 



Diseases of the heart 

Malignant neoplasms 

Cerebrovascular diseases 

Accidents 

COPD* 

Pneumonia and influenza 

Diabetes mellitus 

Chronic liver disease &. 

Atherosclerosis 

Suicide 

All other 

ALL CAUSES 

* chronic obstructive pulmonary disease and associated conditions 
*" cirrhosis of the liver, 19 78 

^/ among Indians and Alaska Natives, "all other" includes 3.3% homicide, and 
2.7 percent deaths attributed to "certain causes of mortality in early 





U.S., 


Indians and 


All 


Races 


Alaska Natives 




38.3 


20.8 




21.1 


10.1 




8.9 


4.8 




5.5 


19.5 




2.6 


0.9 




2.4 


3.8 




1.7 


2.9 


cirrhosis"" 


• 1.6 


6.0 




1.5 


0.7 




1.4 


2.6 




15.1 


28.0// 




100.0 


100.0 



infancy (1978)" 



448 



The distinction between proportionate mortality from heart disease, 
crude, and age-adjusted heart disease rates among Native Americans vs. U.S. 
all races is critical due to the younger age and excess noncardiovascular 
mortality in the Native American population. Disparities in age-adjusted 
rates between Native Americans and whites are most pertinent for this 
report. Unfortunately, of the data suitable for comparison purposes, 
proportionate mortality data were more readily available than age-adjusted 
rates [the Indian Health Service may have more specific recent tabulations 
than those provided to date (2)]. 

As shown in Table 2, Native American rates of infant mortality and 
mortality due to tuberculosis, gastrointestinal disease, accidents, and 
alcoholism have decreased markedly since 1955. However, in 1980 Native 
American mortality from tuberculosis, accidents, and alcoholism was still 
disproportionately high when compared to the general population. Native 
American mortality rates were more similar to mortality rates of other 
non-whites in the population than to rates for whites. Native Americans 
were at somewhat higher risk than other non-whites in 1979/1980 for all 
mortality classes shown in Table 2 except infant mortality. 



Table 2. Comparison of mortality rates for Indians and Alaska 

Natives with those of the general population and other U.S. non 
white populations in two time periods for selected causes @ 



CAUSE OF DEATH 
CLASSIFICATION 



Infant Mortality 



Tuberculosis 



Gastrointestinal 
Disease 

Accidents 



Alcoholism 







RATIO 


TO 


RATIO TO U.S. 




RATE 


U.S. ALL 


RACES 


OTHER NON-WHITES 


1955 


62.7^ 


2.4 




1.5 


1979 


14 . e* 


1.1 




0.7 


1955 


^1.9ij: 


6.9 




2.4 


1980 


3.6i^ 


6.0 




1.5 


1955 


15 . 4''^''^ 


4.3 




2.3 


1980 - 


4 . 0'"^* 


1.3 




1.3 


1955 


184.0#5'^ 


3.3 




2.6 


1980 


107.3#y^ 


2.5 




2.1 


1969 


56.6! 


7.4 




not given 


1980 


41.3! 


5.5 







@ data for Indians and Alaska Natives are based on reservation states. 

* deaths per 1000 live births; from reference 2, Table 3.3 

# age-adjusted deaths per 100,000 population; from reference 2, Table 4.11 
** age-adjusted deaths per 100,000 population; from reference 2, Table 4.13 
## age-adjusted deaths per 100,000 population; from reference 2, Table 4.7 

! age-adjusted deaths per 100,000 population; from reference 2, Table 4.10 



449 



Data on heart disease mortality in the available Indian Health Service 
tabulations covering the time period up to 1979 and 1980 (2) are limited in 
detail. More detail is available in published IHS reports for the period 
up to 1975 (6,8). Using these reports. Tables 3, 4 and 5 have been 
constructed to show time trends in heart disease mortality among Native 
Americans and their relationship to certain trends in other classes of 
death, variations in mortality patterns by region, and age-specific 
patterns vs. those of the total U.S. population. 



Table 3. Percent change in age-adjusted mortality (rate per 

100,000 population) between 1970 and 1975 for Indians 
and Alaska Natives and the U.S., all races (from ref. 6) 



Cause of Death 



Indians and 
Alaska Natives© 



U.S. , 
All Races 



ratio'' 



All Causes 



- 7.3 



■10.6 



1.3 



Disease of the Heart 


-12, 


.7 


Cerebrovascular 


-20, 


.9 


Arteriosclerosis 


-14, 


.4 


Hypertension 


- 5, 


.9 


Diabetes Mellitus 


-12, 


.2 


Homicide 


+19, 


.4 


Suicide 


+45, 


.3 


Cirrhosis of the liver 


+ 7, 


.9 



-13.1 


0.7 


-17.8 


0.8 


-21.4 


1.5 


-34.5 


0.8 


-17.7 


2.1 


+15.4 


2.5 


+ 6.8 


2.1 


- 6.1 


4.4 



@ based on reservation states 

" 1975 ratio of rate for Indians and Alaska Natives to rate 
for U.S., all races. 



Table 3 indicates a decrease in heart, cerebrovascular, and 
arteriosclerosis mortality among Native Americans to an extent roughly 
comparable to that for the general population during the period between 
1970-75 but a substantially lesser decrease in deaths due to hypertension. 
The disproportionate increase in deaths attributed to suicide and liver 
cirrhosis among Native Americans influences interpretation of the decreases 
in the other categories. Similar cardiovascular mortality may not 
represent similar incidence of cardiovascular disease, (e.g., if heart 
disease mortality is pre-empted by competing causes of death). 



450 



Table 4. Age-specific death rates for cardiovascular diseases 
and diabetes for Indians and Alaska Natives (1973-75 
average) and U.S., all races (1974) in 25 reservation 
states (deaths per 100,000 population) (from ref. 6) 



Cause of 








Age Group 




- 


Death 




25-34 


35-44 


45-54 


55-64 


65-74 


Heart 


Ind 


19.6 


65.0 


192.4 


451.0 


1426.6 




US 


9.4 


55.7 


215.5 


590.8 


2758.4 


Hyper- 


Ind 


-- 


1.3 


2.8 


9.2 


9.8 


tension 


US 


0.3 


0.9 


2.0 


4.3 


26.3 


Cerebro- 


Ind 


4.8 


17.2 


47.4 


123.8 


492.7 


vascular 


US 


3.6 


13.3 


35.3 


99.6 


869.0 


Arterio- 


Ind 


1.0 


1.8 


7.8 


23.7 


83.3 


sclerosis 


US 





0.2 


1.0 


5.9 


153.3 


Diabetes 


Ind 


3.8 


15.5 


35.1 


86.4 


171.6 


Mellitus 


US 


1.9 


4.3 


11.4 


31.7 


132.6 



Forty-three percent of the heart disease deaths among Native Americans 
are due to myocardial infarction; 32% are due to chronic ischemic heart 
disease (6) . At all ages below age 35 (ages 1-24 not shown) , the heart 
disease death rate for Native Americans was approximately twice as high as 
for U.S., all races. Above the age of 44, heart disease mortality 
increases less steeply with age in Native Americans than in the general 
population, and Native American rates are lower than U.S. rates for all age 
groups over 45. This cross-over in heart disease mortality is hidden in 
the overall 0.7 ratio of Native American to U.S., all races rates (Table 3), 
since the numbers of deaths at the younger ages are quite small. A later 
cross-over in arteriosclerosis and cerebrovascular disease death rates is 
observed. Native American rates are similar or moderately higher than U.S. 
rates at younger ages (under the age of 65), and substantially lower at 
older ages (over age 65 years). It should be noted that heart disease 
other than ischemic disease (i.e., congenital heart disease) makes up a 
larger proportion of the heart disease under age 35 compared to the 
proportion in older age-groups. Diabetes deaths are higher among Native 
Americans at all ages over 25. 

The differences in the proportion of mortality due to heart disease 
among Native Americans in different regions of the country are shown in 
Table 5. Since the rates for Indian Health Service service areas are not 
age-adjusted, the percent of the population under one year and over 30 
years of age is shown for reference in making comparisons. In 1977, 88% of 
Indians lived in the states where the IHS had responsibility for providing 



451 



health services; 67.5% of the Indians living in these states lived within 
the service unit boundaries (8) . Among the Indians represented in the IHS 
data for 1975-77, heart disease mortality is lowest in the Southwest. 



Table 5. All cause and heart disease mortality and proportionate 
mortality from heart disease in Indian Health Service 
service areas, 1975-1977 (constructed from reference 8) 



Service Area 


% < lyr 


% > 30 


All Causes 


Heart 


% heart 




old 


years old 


/100,000 


7100,000 


1 


All areas 


2.57 


31.0 


751.2 


127.6 


17.0 


Tuscon 


2.68 


30.5 


837.7 


82.8 


9.9 


Aberdeen* 


2.95 


27.9 


1,135.6 


214.6 


18.9(3 


Bemidji"" 


2.31 


30.0 


918.2 


252.7 


27.5 


Albuquerque# 


2.67 


30.3 


648.1 


56.3 


8.7 


Alaska 


2.39 


29.1 


696.5 


84.4 


12.1 


Billings//// 


2.77 


28.6 


869.5 


178.6 


20.5 


Oklahoma City 


1.98 


40.3 


683.6 


190.4 


27.9 


USET! 


2.68 


30.6 


662.7 


111.3 


16.8 


Phoenix! ! 


2.61 


29.2 


751.1 


90.1 


12.0 


Portland+ 


2.57 


33.1 


889.2 


174.6 


19.6 


Navajo++ 


3.07 


25.1 


613.8 


49.8 


8.1 



" North and South Dakota, Nebraska, Iowa 
*" Minnesota, Wisconsin, Michigan 
// Colorado, New Mexico 
//// Montana, Wyoming 

! North Carolina, Florida, Louisiana, Mississippi 
! ! Arizona, Nevada, Utah, California, Oregon, Idaho 
+ Washington, Oregon, Idaho 
++ Utah, Arizona, New Mexico 

(3 rate given in Table 18 (ref 8) is in error, but correct data 
are shown elsewhere in Table 18 and in Table 20. 



When the tabulations of mortality data are taken together, heart 
disease appears to be a significant contributor to mortality in Native 
Americans outside of the Southwest, except Alaska, but proportionately less 
so than for the general population--apparently related to the mortality 
contribution of noncardiovascular causes. The impression gained from 
overall rates of heart disease mortality for the total Native American 
population could be misleading if these two caveats are overlooked: 1) In 
1975-77, Native American rates were lower than those of whites in older but 
not younger age-groups; and 2) the proportion of deaths due to heart 
disease was still relatively low among a large segment of the Indian 
population. 



452 



3.0 ISCHEMIC HEART DISEASE IN SPECIFIC NATIVE AMERICAN POPULATIONS 

3 . 1 Southwestern Indians 

Review of older papers on coronary heart disease (CHD) in southwestern 
Indians aids examination of the baseline from which increases or decreases 
are judged. Although the data bases used have limitations (e.g., 
dependence on hospital cases, autopsy records), the methodologies and their 
limitations are generally well-documented and data-based inferences 
separated from impressions and opinions. Moreover, in many instances, the 
magnitude of differences between Indian and white comparison populations is 
often much larger than the probable error. 

The clinical impression in the 1960 's was of an absence of CHD among 
the Navajo and Apache, based on the failure to observe CHD in Indian Health 
Service hospitals for periods of several years (26,28,31). This impression 
was supported by a prospective study conducted by Cornell Medical School 
investigators in a rural, isolated, traditional Navajo community (Many 
Farms) between 1956 and 1962 (31). With a very high probability that all 
symptomatic CHD in Many Farms was identified during the study period, the 
six year incidence was four in 508 persons. In a comparison with data from 
Framingham (taking age and sex into account) , the CHD incidence was 
significantly less than expected in the Navajo men but not the women. 
Prevalence of hypertension, ECG abnormalities and cigarette smoking were 
also very low in this Navajo population. 

ECG measurements on 70 male and 7 7 female White Mountain Apache Indians 
ages 30 and over in 1957-58 found no records characteristic of coronary 
disease (26). However, a 1957-1966 study of myocardial infarction in a 
large southwestern Indian Health Service population suggests that CHD, 
although of low occurrence, was definitely present to some extent in all 
tribes (23). Rates were approximately one-fourth of Fraraingham-based 
expected rates. One hundred and thirty-eight myocardial infarctions (Mis) 
were identified in an estimated population of 15,905 Indian adults (over 
age 30) at risk vs. 507 expected; only 56 of the 138 Mis were recent. The 
Indian rate was 86 vs. 347.8 (per 100,000) estimated for Framingham 
(estimate based on age and sex, not risk factors) . The sex ratio for MI 
was lower in the Indian populations (2.3:1 vs. 4.6:1 in Framingham), 
possibly related to the high prevalence of diabetes among the Indian women. 
MI rates were higher in the desert tribes (Pima, Papago, Colorado River) 
than in the mountain or canyon tribes (Apache, Navajo, and others). 
Cigarette smoking patterns paralleled the MI patterns. In reporting these 
data Sievers emphasizes that no tribal group is immune from CHD, as had 
been implied in some earlier reports. 

More recent studies among the southwestern Indians suggest that CHD 
is increasingly less rare, particularly when diabetes is present (3). 
However, a 1976 report points out that CHD incidence in both diabetic and 
nondiabetic Pima Indians was lower than among white comparison populations 
(ECG data (Q wave changes) on 85% of half to full-blooded Pimas on the Gila 
River Reservation (46)). Sievers (47), as noted below, describes 
increasing rates of ischemic heart disease in Indians. In contrast, Kunitz 



453 



indicates that ischemic heart disease, although not unknown, is rare among 
the Navajos compared to the U.S. general population--citing autopsy, 
hospital, and community studies through 1967 (11). This rarity has been of 
particular interest to some investigators due to the use of substantial 
quantities of saturated fat in the traditional Navajo foods. Kunitz also 
states that "there is no evidence to indicate that the rate of myocardial 
infarctions has increased during the 1970's" (11; p. 98). He cites 
relevant numbers of hospitalizations and deaths in support of this 
impression, but he gives no denominators. An average annual mortality rate 
(presumably age-adjusted and due to MI) of 12 to 14 for Navajos vs. 158.7 
for the white population was cited. Earlier in the same chapter, estimated 
mortality due to diseases of the heart is given as follows: 

1954-56 29-34 per 100,000 

1965-67 42-49 per 100,000 

1973-75 46-53 per 100,000 for the Navajo area 
(which includes the Hopi reservation for the first two time periods) vs. 
216.7 per 100,000 for the U.S., all races in 1976 (11) (whether the Navajo 
rates are adjusted to the U.S. age distribution is not clear). These rates 
could be interpreted as showing an increase--particularly if subtraction of 
the Hopi data lowers rates for the earlier time periods. 

Sievers and Fisher, in a summary of diseases which occur in unusually 
high or low frequency among North American Indians, include CHD as a 
condition which is relatively "uncommon among full-heritage southwestern 
American Indians' , in spite of high rates of diabetes mellitus, obesity, 
and moderate, increasing rates of hypertension (3). These authors cite 
age-sex-adjusted acute myocardial infarction mortality rates as follows'^- 

U.S.-all races 152.4 per 100,000 

U.S. -all Indians 135.0 per 100,000 

southwestern Indians 14.7 per 100,000 and attribute the 
lower rates among southwestern Indians in part to a lesser degree of 
non-Indian admixture and acculturation compared to Indians elsewhere in the 
U.S. (6). Possible determinants of this lower CHD are lower plasma 
cholesterol levels, higher ratios of high-density lipoprotein cholesterol 
(HDL-C) to low-density lipoprotein cholesterol (LDL-C), lower prevalence of 
cigarette smoking, infrequency of interpersonal competitiveness, and higher 
frequency of blood group among southwestern Indians --all of which are 
associated with reduced CHD risk. The impression of these authors is that 
increases in CHD in various Indian tribes are commensurate with tribal 
changes in lifestyle and increased diabetes and hypertension (3) . 

Sievers and Fisher (3,47) offer the data in Table 6 to illustrate 
differences in rates of increase of acute myocardial infarction over time 
in different tribal groups. The validity of the differences shown would 
depend upon the equivalence and freedom from sample bias in the data for 
the two time periods and in the three tribal groupings. Assuming that 
there are not major problems in the data, the trends indicated are striking 
and suggest that CHD will be increasingly seen among southwestern Indians. 
The authors note that "duodenal ulcers have exhibited a similar tribal 
pattern of increase" (3, p. 210). 



454 



Table 6. Comparison of rates of acute myocardial infarction 
during 1957-66 vs. 1975-78 in three sub-groups of southwestern 
Indians (taken from 3,47) 



Piman 

(Pima and Papago) 

Athapascan 

(Navajo and Apache) 

Other 
Southwestern" 



rate per 100,000 per year 
1957-66 1975-78 
50 74 



18 



33 



53 



97 



/o increase 
48% 

194% 

194% 



" In the text accompanying these data, the authors note that 
35% percent of the infarctions in this category were among 
Hopi Indians, who are only 19% of this group 



3.2 Indians Outside the Southwest 

Mayberry and Linderaan examined cardiovascular disease death rates 
among Seminole Indians integrated into the Seminole County, Oklahoma 
population vs. those of whites in the same county (36). The authors note 
that in addition to other limitations of death certificate data, 
mixed-heritage Indians may have been recorded as either Indian or white on 
death certificates. The percent of mortality attributed to coronary artery 
disease (using data for persons age 25 and over) was less among the 
Seminoles than among whites (15.5 vs. 31.0% for men; 11.1 vs. 20.7% for 
women) (36, table III). Coronary artery disease (CAD) death rates 
calculated from Table III are as follows: Seminole males 15.5/1000; white 
males 37.5/1000; Seminole women 8.4/1000; white women 14.1/1000. 
Tabulations of death rates for male Indians aged 25 and over in other 
Oklahoma counties showed proportionate CAD mortality ranging from 12 to 33% 
(36, table IV), varying with the overall mortality pattern for the Seminole 
men in the different counties.- These data demonstrate higher CAD mortality 
among Seminoles than among southwestern Indians at approximately the same 
time period. 

Pinkerton and Badke (34) retrospectively determined the incidence of 
myocardial infarction (MI) among Crow and Cheyenne Indians admitted to Crow 
Hospital (Crow Agency, Montana) during the 14-year period from 1956 to 
19 70. The study methodology was designed for comparability with the 
14-year Framingham data, to the extent possible. Of the CHD categories 
ascertained, the authors were most confident of the completeness of the MI 
data (compared to angina pectoris, for example, which may have been treated 
primarily on an outpatient basis). Therefore, the authors base their 



455 



conclusions on the MI data. In calculating denominators for MI rates, 
off-reservation Indians who lived too far away to be in the hospital 
service population were excluded. Otherwise, maximum estimates of 
populations of Crow and Cheyenne men and women at risk were used so that 
the rates calculated would be conservative (i.e., if in error the rates 
would underestimate rather than overestimate the incidence of MI. The 
racial criterion in the tribal census was one-quarter or more Crow (this 
may also have applied to the Cheyenne) . 

Equivalent or higher MI rates for Crow men and both Crow and Cheyenne 
women vs. rates for Framingham age-sex counterparts (10-year age-groups 
between 30 and 59) were reported. Indian women had MI rates at least twice 
as high as Framingham wo'ien at all ages, and had rates six times higher in 
the 45-54 year age-group. 

Rates for Cheyenne men were substantially lower than those of the Crow 
and Framingham men. When maximum Framingham rates were calculated assuming 
that all persons excluded at the first exam due to known CHD had had 
infarctions during the subsequent 14 years, Framingham MI rates for men 
were significantly higher than for both Crow and Cheyenne men. Rates among 
women were not significantly different using the upper limit Framingham 
rates. As noted above for the Seminole Indians, rates for Crow and 
Cheyenne Indians were higher than those reported for southwestern Indians . 
Pinkerton and Badke point out that their findings were contrary to the 
clinical impression of the Crow hospital staff that infarction was rare 
among Crow and Cheyenne Indians . 

Gillum et al . (33) report that cardiovascular disease was the leading 
cause of death among Minnesota Indians (primarily Chippewa) between 1968 
and 1973 with rates comparable to those for Minnesota whites (age-adjusted 
rates for heart disease and stroke combined: 448.7/100,000 for Indians 
455.2/100,000 for all races; proportionate mortality 26% among Indians). 
These authors draw attention to the similarity in heart disease and stroke 
mortality rates between Indians and whites vs. the substantially higher 
age-adjusted total mortality for the Indians (due to excesses in other 
categories. Thus, this is an example of similar cause-specific rates but 
lower proportionate mortality. Fifty-six percent of Minnesota Indians 
lived in urban areas in 1970. Rates in reservation and urban areas were 
similar. 

3 . 3 Summary 

These studies of CHD in specific populations, although neither 
comprehensive nor up-to-date, confirm the general impression that CHD is 
lower among Indians in the Southwest than among Indians elsewhere and that 
patterns for Indians elsewhere are similar to those of whites in the same 
areas. Also, the higher heart disease death rates among Indians in IHS 
health service areas in 1973-75 vs. the U.S. general population through age 
45 may suggest higher risk in younger cohorts (Table 4). However, the 
proportions of ischemic vs. other forms of heart disease at the younger 
ages are not clear. 



456 



Due to marked differences in the risk of death from other causes 
among Native Americans and whites, proportionate mortality figures, which 
are relative, tend to minimize the potential importance of heart disease 
risk. The overall impression of lower heart disease mortality among Native 
Americans (1975 ratio to U.S., all races = 0.7) may be influenced downward 
by the lower rates in the Southwest where the majority of Indians live. 
The CHD picture for Indians outside of the Southwest may be less favorable. 

There are many as yet unresolved issues related to CHD in Indians. 
Those encountered most often are issues of measurement (e.g., appropriate 
interpretation of ECG findings (46)); risk factor-disease associations 
(e.g., obesity and diabetes on CHD (13,20); consequences of hypertension 
(45)); and heredity-environment interactions (20,25). 



4.0 ISCHEMIC HEART DISEASE RISK FACTORS AMONG NATIVE AMERICANS 

4.1 General Comments 

Lifestyle-related risk factors appear to have increased substantially 
in Native American communities in the last 50 years with increasing 
urbanization and acculturation (3,33,45). However, in the absence of 
systematic risk factor surveys among most Indian populations, 
quantification of these risk factor changes is difficult. Some apparent 
increases are possibly due to increased screening efforts (45). 

In addition to personal and environmental factors which affect IHD risk 
factor trends in the general population, risk factor changes of Native 
Americans vary with tribe (both hereditary and cultural factors), extent of 
admixture for Indians who are not full-heritage, extent and duration of 
acculturation to white society, and regional factors (e.g., origins in the 
Southwest vs. in Seattle, Minnesota, or upstate New York (3,45)). The 
picture is further complicated by the differential rates of change of the 
admixture and acculturation variables in different Indian communities and 
by the different socioeconomic and quality of health care patterns for on 
and off-reservation Indians (45). The variation is both qualitative and 
quantitative; summary statements about IHD risk in Native Americans can 
only be made within groups with similar origins and experiences. 

4.2 Hypertension 

Mortality attributed to hypertension and stroke was lower than that 
for heart disease in the IHS health service areas in 1973-75 (Table 4). 
However, between ages 25 and 64 years, rates among Indians were similar to or 
higher than those for the general population. Thus, hypertension is not 
inconsequential in the Native American population and it may increase in 
importance as other causes of mortality decline. 

At the 1977 conference on hypertension control in Native American 
communities, Maurice Sievers, M.D. , Director of Research for the Phoenix 
Indian Health Service Area presented an historical overview (and critique) 
of reports of hypertension among American Indians and Alaskan Natives (45, 



457 



pp. 77-82). Dr. Sievers notes the inadequacy of the "numerous bits of 
information" on this subject. Several speakers at this 1977 conference 
noted that the extent of the problem of hypertension among Native Americans 
was not at all well-documented. Dr. Sievers points out that the data which 
are available are often difficult to identify; they are buried within 
studies of diabetes or other aspects of Indian disease. He also points out 
that there are major tribal differences in cardiovascular disease, 
including a higher prevalence of congenital cardiovascular abnormalities in 
the Athapascans (Navajo and Apache) than in other tribes. 

Highlights of Dr. Sievers' summary follow--grouped by tribe and region 
to the extent possible. The talk by Sievers (45) is reported without 
citations. Reference 48 is a documented version of this text. Where the 
study described was recognized as one included in the bibliography for this 
report, a notation to this effect has been made in parentheses and the 
impression conveyed in Sievers' report verified by examination of the 
primary data. 

Regarding southwestern Indians: 

- a rate of hypertension among Navajo Indians less than one-fourth 
the white rate was reported in 1948-52; 

- 6 . 2% of the men and 3.7% of the women ages 30 and over in the 
Cornell -Navajo 1956-62 study at Many Farms Arizona (reference 31) 
were hypertensive; 

- a 1970 report indicated that migration to an urban environment was 
associated with higher blood pressures among Navajo men (49); 

- 1.4% of admissions to the Phoenix Indian Medical Center in 1953 had 
primary hypertension (based on one, unstandardized casual blood 
pressure reading) ; 

- hypertension-related morbidity among Phoenix-area outpatients in 
1952 was 7 per 1,000 for Papagos , 4 per 1,000 for Pimas, and 2 per 
1,000 for Apaches vs. 25 per 1,000 for whites. Two-fifths of the MI 
cases identified in a 10-year study (1957-66) (23) were hypertensive; 

- an analysis of computerized clinic records of more than 4,000 Papago 
Indians for the period 1969-1972 yielded a hypertension prevalence rate of 
20% (Sievers notes, however, that the methodology used has rather serious 
limitations); the prevalence of hypertension and complications was greater 
in hypertensives who also had diabetes; 

- blood pressures of Pima Indians studied by Ingelfinger 

(46) were lower compared to whites but were higher in diabetic 
vs. nondiabetic Pimas; 



458 



- Leo observed a 34% prevalence of diastolic blood pressure greater than 95 
mmHg among White Mountain Apache men and a 29% prevalence among the women 
(28) in a 1958 study of 110 men and 110 women volunteers; 

- Clifford et al. also noted a high prevalence of hypertension among 327 
White Mountain Apaches studied in 1963 (26% in men, 23% in women) (26); 
examination of the Clifford et al. data indicates particularly high 
hypertension prevalence (BP >160/95) in Apache men ages 30-49 (43-47% vs. 
rates of 12-23% among older men). Highest rates among Apache women were in 
the 50-59 year old group (Figure 1 in reference 26)). 

Regarding Indians outside of the Southwest: 

- a systematic study of blood pressure found a very low rate of 
hypertension (1 in 200 Indians over age 20) in a northwestern coastal 
village; 

- A blood pressure survey of Seminole Indians in Seminole County, Oklahoma, 
Seminoles on a reservation in Florida, and Seminole County whites indicated 
similar blood pressure levels among the three groups (36); 

- no differences in blood pressure levels were observed among Sioux and 
white admissions to a South Dakota hospital (50 consecutive admissions of 
each race) in spite of the fact that 50% of the Sioux vs. 10% of the whites 
were diabetic (and most of the Indians were overweight). 

Regarding Eskimos and Alaska Natives: 

- 2.6% of 842 Eskimo men surveyed by Scott et al . (50) in 1958 had a mean 
blood pressure of 125; blood pressures were similar to those in a large 
group of U.S. men. 

Sievers' account of hypertension studies gives an adequate impression 
of the patterns of hypertension among Native Americans to the limited 
degree that these had been documented up to the mid 1970's. Hypertension 
has previously been relatively infrequent in southwestern Indians-- White 
Mountain Apaches excepted. No striking excess prevalence of hypertension 
in Indians outside of the Southwest (vs. whites in the same areas) has 
been reported. 

Sievers notes that the Indian Health Service age-adjusted death 
rate for hypertension for Native Americans in 1971 was lower than the rate 
for white Americans by only 10% (45). NCHS estimates of mean blood 
pressure levels for American Indians (of f -reservation only) in 1971-74 do 
not show a consistent pattern of differences from blood pressure levels of 
whites (see Tables 7 and 8). However, given earlier statements about the 
intertribal differences and the substantial proportion (60%) of Indians 
still on reservations in 1970 (45) the value of the NHANES data may be 
limited to showing that there were no large differences in off-reservation 
Native American vs. white blood pressure distributions in 1971-74. 



459 



Table 7. Systolic and diastolic blood pressure levels of American 
Indian men, with comparison values for white men, 
U.S., 1971-1974. (from reference 43) 



Systolic 
Indian* White 



Diastolic 
Indian* White 



Age 




(mill 


Group 






18-24 


121.2 


123.7 


25-34 


128.0 


125.2 


35-44 


127.7 


127.0 


45-54 


130.9 


134.7 


55-64 


139.4 


139.6 


65-74 


139.9 


146.0 



(millimeters of Hg) 



77.7 


76.4 


76.5 


80.8 


84.9 


84.2 


89.8 


87.5 


85.4 


86.4 


84.9 


84.9 



examinees who identified themselves as American Indians and 
were not living on a reservation or in an institution at the 
time of the survey 



Table 8. Systolic and diastolic blood pressure levels of American 
Indian women, with comparison values for white women, 
U.S., 1971-1974. (from reference 43) 





Syst( 


3lic 




Indian* 


White 


Age 


Women 


Women 
(mill 


Group 






18-24 


114.9 


115.1 


25-34 


119.0 


116.2 


35-44 


117.4 


122.6 


45-54 


138.9 


131.1 


55-64 


144.3 


143.0 


65-74 


145.0 


151.6 



Diastolic 




Indian* 


White 


Women 


Women 



73.8 


71.3 


75.0 


74.6 


77.6 


79.3 


80.1 


82.6 


88.6 


86.2 


81.5 


85.4 



examinees who identified themselves as American Indians and 
were not living on a reservation or in an institution at the 
time of the survey 



460 



Only three recent reports of hypertension surveys in Indian 
populations were identif ied--two from Minnesota (33,51) and one among 
Navajo (27). 

The Navajo survey reported blood pressure data from 1977 clinic-based 
screenings of Navajo people ages 20 years and older at Fort Defiance, 
Arizona and Crownpoint, New Mexico--two demographically similar Navajo 
communities (n=640) (27). The populations were relatively diverse but were 
not randomly selected. Blood pressure levels of the Navajo women showed a 
linear increase with age. There was no age trend in either systolic or 
diastolic blood pressure among the Navajo men, but their blood pressure 
levels and hypertension prevalence were greater than among Navajo women. 
The prevalence of DBP >=90 was higher among the Navajo men ages 20 to 59 
(24 to 28%) than among the small number of men aged 60 years and older 
(16%). The pattern was similar among the women. Prevalence of DBP >=95 
was 9, 16, 8, and 11% in the 10-year age-groups of Navajo men between 20 and 
59 years of age; 0,8,3, and 10% among the women. One hundred and ten of 
the Navajo screened had DBP >=90, of whom 57 reported a prior knowledge of 
having high blood pressure. Eighty and 72 percent of the Navajo men and 
women on medication had DBP less than 95 mmHg. The authors note that the 
estimates of hypertension are based on one casual reading and are thus 
probably overestimates. 

In an analysis of determinants of blood pressure levels in these Navajo 
subjects, male sex, obesity and alcohol were found to be important 
variables (alcohol use was measured only as yes or no) . Overweight was a 
statistically significant hypertension risk factor for both men and women. 
Relative risks were estimated as 3.0, 3.6, and 9.0 for overweight females, 
normal weight males, and overweight males if normal weight females were 
assigned a value of 1.0. The highest reported use of alcohol was among the 
younger men (43% of men under age 40 vs. 22% of those over 40). The 
prevalence of DBP >=90 was significantly higher among the men who used 
alcohol. Very few Navajo smoke and smoking was not a determinant of 
hypertension. An index of acculturation was not significantly related to 
blood pressure levels (this index included ratings on alcohol use and 
smoking) . 

In their discussion, DeStefano et al . (27) compare the Navajo blood 
pressure levels in 1977 with levels in the 1956-62 Many Farms Study (31) 
for an impression of changes in blood pressure over time. Blood pressures 
of Navajo females were essentially the same at both points in time. Blood 
pressures of the younger Navajo men measured in 1977 were higher than those 
of the men measured in 1956-62 at Many Farms. The authors suggest that a 
trend towards increasing hypertension may be present in the younger cohort 
of men. The 1977 data were also compared with blood pressure levels of 
black and white men in a 1973-75 study of one million Americans. Again, 
the trend towards hypertension in the young Navajo men was apparent. 
Systolic and diastolic blood pressure levels and the prevalence of DBP >=90 
were equal to or greater than levels of young black and white males in the 
mid 70' s. Although this trend in the younger cohort of Navajo men is 
presumably associated with some aspect of acculturation, the nature of such 
an acculturation factor was not evident from the measures used in this 



461 



study. Alcohol use may be an important factor. Blood pressures of the 
Navajo women are lower than those of women in the comparison populations. 

Gillum et al. reported on a blood pressure survey of essentially all 
first, second, and third grade children in the Minneapolis Public Schools 
(who were not absent from school on the day concerned) during the spring of 
1978 (51). The population of 10,640 6- to 9-year old children surveyed 
included 307 Native American children. Analyses of the blood pressure data 
indicated higher systolic (by 1-3 mmHg) and lower 4th and 5th phase 
diastolic (by 2-5 mmHg) blood pressures (and higher pulse pressures) among 
the Native American vs. the white children. The systolic blood pressure 
differences were statistically explained by higher body mass index of the 
Native American children. No good explanation for the lower diastolic 
blood pressure among Native American children could be uncovered. Several 
methodological explanations were tested and ruled out (51). 

Gillum et al . have also reported on a blood pressure survey among 
adult Indians in Minneapolis in 1980-81. Two populations of Indians were 
reached- -one in an Indian housing project (n=173) and the other through 
community screenings (n=295) during American Indian Week (33). Comparison 
data for whites were taken from the Minnesota Heart Survey (probability 
sample) (clinic measurements; n=1950) . 

Self-reported prevalence of hypertension was somewhat higher among 
Indians than whites (33% vs. 27%), but unlike whites who reported a 
positive history, the Indians with a positive history were more likely than 
whites with such a history to have blood presssures in the normal range. 
This discrepancy was not fully accounted for by the proportions of Indians 
and whites on medications. The prevalence of hypertension (defined as 
diastolic blood pressure >=90 mm Hg or diastolic blood pressure <90 but 
taking blood pressure medication) was 13-17% among the Indians and 14% in 
whites. Levels of control among Indians and whites on medication were 
similar. A smaller proportion of Indians than whites with a history of 
high blood pressure were on medication; a larger proportion were on special 
diets (33). 

Ten percent of Indians reporting a history of high blood pressure also 
reported a history of diabetes. Diabetes, smoking, and obesity were more 
prevalent among Indians than whites. Systolic and diastolic blood pressure 
were significantly correlated with the body mass index (coefficients were 
0.33 and 0.36 (33) in the Indians). The overall impression was that blood 
pressure levels of Indians and whites were similar, but that associated 
risks were higher in Indians due to higher prevalences of obesity, smoking 
and diabetes . 

These later studies add to the evidence that 
obesity- and diabetes-related hypertension is an important health problem 
in Indians and suggest the need for more systematic and careful studies of 
blood presssure levels and trends in different Indian communities. 
Attention to trends in younger cohorts seems particularly important 
(26,27). The workshop summaries in the 1977 conference report (45) do not 
contain data on hypertension prevalence (except in references to various 



462 



studies). However, this report is a useful point of reference for issues 
of Native American health services in general and hypertension control 
issues in particular. Many of the relevant research and data needs have 
already been identified and attention to some of these needs may already be 
underway. However, the picture obtained from literature identified in 
conjunction with the present report does not appear to have changed much 
from that reported at the 1977 conference. 

4.3 Cholesterol 

Comparisons of cholesterol levels of Native Americans vs. whites 
indicate lower or similar levels in Native Americans. In a 1968 report of 
cholesterol levels of 746 southwestern Indians compared with 70 
nonsouthwestern Indians and 163 whites, Sievers observed lower levels in 
both groups of Indians compared to whites, no increase in cholesterol 
levels with age, and no sex differences (peak levels between ages 30-44) 
(29). Cholesterol determinations were for Phoenix Public Health Service 
hospital patients over the age 15 during the period July, 1963 through 
December, 1965. The lowest levels were observed among Pima and Papago 
Indians . Pima and Papago Indians had lower cholesterol levels than Apache 
and Navajo, in spite of greater obesity among the Pimans. In a separate 
report, Sievers also comments on the paradox of lower cholesterol levels 
among the Pimans vs. Navajo and Apache in light of the higher frequency of 
myocardial infarction among Pimas (23) . 

Cholesterol levels for nonsouthwestern Indians were slightly higher 
than for southwestern Indians but still lower than those of whites (29). 
For example, among 45-59 year old men in the study, mean cholesterol level 
was 193.7 for southwestern Indians; 214.7 for nonsouthwestern Indians; 
302.8 for whites (levels for whites were duplicated in outside laboratories 
because they seemed unusually high; however, the levels of the Indians 
would have been significantly lower even if the levels for whites had been 
substantially overestimated). 

Hamman et al., in a 1975 report (52) noted similar cholesterol levels 
in 148 pre-menopausal (ages 35-54) and 75 age-matched post-menopausal Pima 
women. Similar pre- and post-menopausal cholesterol levels in women were 
also observed in 65 women followed longitudinally. The findings were not 
affected by the presence of diabetes. Cholesterol levels of males were 
also measured in the cross -sectional survey. The levels of Pima males and 
females were 20-30% lower than those of Caucasians and did not rise with 
age. A 1976 report of serum cholesterol levels in Pima children and adults 
indicates that levels of Pima and white children are similar at birth but 
that levels among the Pima remain low and do not rise with age in adulthood 
(17). 

Ingelfinger et al. (46) reported mean cholesterol levels of 189 and 188 
mg/dl for nondiabetic Pima men and women over age 40 and slightly higher, 
but still low, levels for diabetic Pimas (197 and 198 mg/dl for men and 
women) , with no age-related changes in either group. The most recent 
report of cholesterol levels in Pimas (from the same laboratories) presents 
data collected between 1979 and 1982 (14). Although levels in Pimas are 



463 



lower than those of the Lipid Research Clinic whites, the finding of an 
increase in plasma cholesterol with age in Pima women is a departure from 
the previous findings that no such rise occurred. It is not clear whether 
this is due to sample factors or to a "westernization" of cholesterol 
levels among the Pima women. Levels in men peaked in the 45-54 year age 
group and then tapered off. HDL cholesterol levels were similar in Pima 
males and women. The lack of a gender difference was not explained by 
obesity although obesity and HDL levels were negatively correlated. 

The fat content of the traditional Pima diet is primarily animal fat 
(from beef and pork) . Meat consumption (and thus the percentage of fat 
calories) in the traditional Pima diet was relatively low compared to 
typical U.S. diets (29). However, Savage notes that the cholesterol levels 
of Pima remained lower than those of whites at a point when the usual Pima 
diet had become quite similar to that of the general population (17). 
Metabolic studies in Pima volunteers suggest that there are significant 
differences in apoprotein and lipoprotein metabolism which may account for 
the different lipid profiles of Pima Indians (15,24). The high prevalence 
of gallstones among southwestern Indians, including the Pima, has been 
suggested as a possible explanation for the lower blood cholesterol levels 
(3,11); however, this view is not widely supported. 

The 1956-62 Many Farms Study among the Navajo indicated relatively low 
cholesterol values in 89 and 113 randomly-selected men and women for whom 
cholesterol determinations were made (31). The authors were reluctant to 
generalize to the Navajo as a whole, partly because of their belief that 
the Navajo diet was high in saturated fat. In fact, the study was 
motivated by what appeared to be a paradox of high fat intake and low CHD 
in this population. Although fat from mutton or lard is an important part 
of traditional Navajo food, other authors, including Keys (25,26) have 
pointed out that the total percent fat in the Navajo diet was around 24%, 
much lower than the 40% typical of Americans in general. Also, dairy fat 
is not common in the Navajo diet (26) . 

Two studies among the White Mountain Apache (26,28) indicated low 
cholesterol levels in this group (in the range of 185 to 200 mg/dl) 
compared to whites. However, Clifford et al. noted a lower percentage of 
cholesterol levels under 225 mg/dl among younger Apache men ages 25-44 vs. 
45-64 year old men (72% vs. 86%) and commented that cholesterol patterns in 
the younger Apache men might be changing (26) . 

In the study of Seminole Indians in Oklahoma (36), the prevalences of 
serum cholesterol >260 mg/dl were 9.1% and 5.4% in Seminole men and women 
vs. 15.6 and 9.1% in white men and women. The authors attribute most of 
this difference to the younger ages of the Seminoles in their sample and 
state that the overall serum cholesterol distributions were similar. 

The Minnesota study (33) is the only recent report of cholesterol 
levels among Indians other than Pimas which could be identified. Total 
cholesterol levels of the Minneapolis Indians were similar to those of 
whites under age 55 and lower after age 55. HDL cholesterol levels of 
Indian and white men were similar; lower HDL levels among the Indian vs. 



464 



white women were noted, particularly after age 55. The prevalence of serum 
cholesterol >230 mg/dl was 9% in the 213 Indians with complete lipid data. 

Scott et al. (50) reported on cholesterol levels of 842 Eskimo men in 
the Alaska national guard. Mean cholesterol level was 214 mg/dl. The 
authors emphasize that there was considerable regional variation. In 
defending the cholesterol-CHD hypothesis against assertions that Eskimos 
have a high fat diet but little atherosclerosis, Keys points out that 
neither the overall fat content of the Eskimo diet nor the absence of 
atherosclerosis among Eskimos has been documented (25). 

It is clear that serum cholesterol levels among some American Indians 
are lower than in the general population but the relationship of these 
lower levels to CHD incidence is not clear. Nor are the trends in 
cholesterol levels with increasing acculturation, racial admixture and 
urbanization well defined. These issues should be addressed as a part of 
an overall effort to follow IHD risk factor trends in this population. 

4.4 Smoking and Alcohol Use 

Sievers documented cigarette and alcohol use patterns among American 
Indians in a 1968 report based on interviews of patients at the Phoenix PHS 
Hospital between 1961 and 1965 (22) . His findings can be summarized as 
follows: heavy cigarette usage (>1 pack per day) was rare among 
southwestern Indians (4.4. and 1.3 percent in males and females); smoking 
habits of nonsouthwestern Indians were similar to those of the general 
population; Indian women outside of the southwest were more likely than 
white women to be heavy smokers. Heavy alcohol usage (>1.6 ounces of 
absolute alcohol more than once per week) was most common in southwestern 
Indians but similar in nonsouthwestern Indians and significantly greater 
in both groups of Indians than in whites (the white comparison group was 
taken from a study of drinking in Iowa) . Both heavy cigarette and alcohol 
use were more frequent among men than among women in all groups studied. 
Among the southwestern Indians, heavy smoking was least common among the 
Apache and Colorado River Indians, more common among Pima and Hopi and most 
common among the Navajo and Papago. However, all rates among southwestern 
Indians were much lower than for the general population and for 
nonsouthwestern Indians (range of to 6% in the Southwest vs. 20-26 
percent in the other two groups). The tribal patterns of heavy alcohol use 
were different from cigarette use patterns. Of the tribes discussed in 
this report (i.e., excluding some smaller tribes). Apaches were most likely 
to be heavy alcohol users, Navajo and Colorado Indians next most likely, 
Pima and Hopi least likely. 

Smoking among the Many Farms Navajo (1956-62) was assessed by interview 
of a random sample of 55 families (74 individuals) (31). Forty-one of 74 
people interviewed were nonsmokers and another 26 smoked 2 to 5 cigarettes 
per week. None of the people surveyed smoked more than one pack per day. 
In the later (1977) study among the Navajo (27), 13% were smokers and 94% 
of these smoked less than one pack per day. Forty-percent of the Navajo 



465 



men under age 40 compared to 22% over age 40 reported using alcohol in the 
1977 study. The authors noted that this may have indicated a trend towards 
higher alcohol use in the younger cohort. Ingelfinger reported that only 
2.5% of Pima males and no Pima females smoked more than one pack of 
cigarettes per day (46) . 

In contrast, smoking was highly prevalent among the Minneapolis 
Indians surveyed by Gillum et al. in 1980 (33). However, this probably 
does not represent a trend towards increased smoking among the Chippewa. 
According to the authors, smoking has been highly valued in traditional 
Chippewa culture. Seventy-seven and sixty-seven percent of the Indian men 
and women surveyed were current smokers ; 45% smoked more than 20 cigarettes 
per day (there was no sex difference in number smoked per day) . Of those 
who smoked, only 25% reported wanting to stop smoking, although most had 
tried to quit. Reported alcohol intake in the Minnesota population was 
low. Forty-eight percent reported abstinence; those who drank reported 
consumption of alcohol at least two days per week. 

Cigarette and alcohol use of 76 Native American students in the 
University System of Georgia were ascertained in a 1972 study of 20,547 
students (41) . Reported cigarette use among the Native American students 
was highest of all the ethnic groups (white, black, Asian, other) and 
reported alcohol use was second highest. A 1973 study of drug use patterns 
among American Indian and white high school students in Wyoming reported 
more favorable attitudes towards drug use among the Indian students, but 
alcohol was not among the drugs specifically queried (35). In a survey of 
students between 10 and 20 years of age in Anchorage Alaska, Native 
American students (5.7% of 15,634 respondents) were less likely than white 
students to be nonusers of any drugs and more likely than any of the other 
ethnic groups to have tried drugs in addition to alcohol or tobacco (37). 

The association of cigarette and alcohol use with IHD risk among 
Native Americans has apparently not been explored, although the social and 
other health consequences of heavy alcohol use in Indian populations have 
received great attention in the Native American literature (3,53). 
Insufficient data are available to draw any conclusions about trends in 
these variables or their contributions to IHD patterns. 



5.0 MULTIVARIATE PERSPECTIVE 

A discussion of obesity and diabetes among Native Americans is beyond 
the scope of this paper. However, it is appropriate to draw attention to 
the apparently large public health importance of these two conditions in 
most Native American populations and to their enhancement of what might be 
(for many tribes) an otherwise relatively benign IHD risk profile. A 
greater prevalence of obesity in American Indians vs. whites was mentioned 
in the majority of papers reviewed (7,11,12,20,23,26,27,30,31,33,36,39,40, 
45,46,48,49,51) and in others not noted above (54-57). Two papers (39,40) 
note the excess prevalence of obesity among Seneca Indians--a group for 



466 



whom other papers related to IHD risk were not identified. The mortality 
risk associated with obesity among Pima Indians does not appear to be the 
same as for the general population (20). 

The excess risk of diabetes among Native Americans is evident in the 
mortality data. The Pima Indians have an unusually high prevalence of 
diabetes, but an excess of glucose intolerance prevalence is apparently 
typical of many adult Indian populations (3,12,13,20,33,36,39,40,46). The 
absence of diabetes among the leading causes of death for the Navajo (11) is 
consistent with a low or moderate prevalence of diabetes among some 
Athapascan tribes (Navajo and Apache) (3,23) . Diabetes is reportedly common 
in Apache tribes in Oklahoma (3) . 

From a multivariate perspective. Native Americans are at high 
potential IHD risk. With the exception of elevated cholesterol and 
smoking, standard risk factors and predisposing co-morbid conditions are 
equivalent or higher in American Indian populations where comparisons have 
been made. This suggests that the future of IHD risk may become worse for 
American Indians at a time when the picture is improving for large segments 
of the general population. 



6.0 IMPLICATIONS AND RECOMMENDATIONS 

To draw conclusions about current IHD risk perspectives among Native 
Americans on the basis of the limited data available would be 
inappropriate. Probably there is no one conclusion that will apply to all 
Native American people; there are at least two distinct patterns implied. 
Indians in the Southwest have lower overall IHD risk than Indians in other 
parts of the country. However, Native Americans in all parts of the 
country may have excess IHD risk associated with excess obesity and 
diabetes. In some areas of the country Native Americans are at excess IHD 
risk due to lifestyle factors (cigarette use) . Although the risk of 
hypercholesterolemia among Native Americans may be lower than in the 
general population, in no sense does this result in "immunity" to IHD. 

In spite of an impression from available literature that IHD is not an 
important contributor to overall Native American-white mortality 
disparities (due to extreme disparities in certain other mortality 
classes), the fact that heart disease is the leading cause of death among 
Native Americans must be kept in mind. Moreover, there is evidence of 
excess heart disease mortality among Native Americans at younger ages. 

In conclusion, the following recommendations are put forth: 

--systematic data collection is needed, if not tribe-specific 
then at least specific to major subgroups which show different 
risk patterns (e.g.. Southwest vs non-Southwest); 



467 



-more of the Indian Health Service data should be included 
in frequently used publications of health statistics; 

-intervention on those risk factors already identified is indicated, 
particularly prevention of obesity and diabetes; the disparities 
in this area are huge and are bound to result in increasing 
health problems for Native Americans as their life span increases 
and deaths from other causes are reduced. 



ACKNOWLEDGEMENTS 

We gratefully acknowledge the editorial assistance of Sandra 
J. Anderson and Elisabeth Pitt. 



468 



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1. DHHS. Task Force on Black and Minority Health. Black-White 
Mortality Cross Over. TFBMH/CHPatrick 7/12/84 

2. DHHS. Indian Health Service. Indian Health Service Chart 
Book Series. June 1984. (excerpts only) 

3. Sievers ML, Fisher JR. Disease of North American Indians. 
IN Rothschild HR, ed. , Biocultural Aspects of Disease. 
New York: Academic Press, 1981, Chapter 8, pp. 191-252. 

4. Gonzalez NL. Changing dietary patterns of North American 
Indians. In Moore WM et al., eds . Nutrition, Growth, and 
Development of North American Indian Children. Washington, D.C, 
U.S. Governmnent Printing Office. DHEW Publication No. 

(NIH) 72-26, 1972), pp. 15-33. 

5. Taylor TW. The States and Their Indian Citizens. United 
States Department of the Interior. Bureau of Indian Affairs. 
Washington, D.C. 1972. 

6. U.S. Department of Health, Education, and Welfare. The 
Indian Health Trends and Services. U.S. Government Printing 
Office. Washington, D.C. 1978. HSA 78-12009. 

7. Sievers ML. Disease patterns among Southwestern Indians. 
Public Health Reports 1966;81:1075-1083. 

8. U.S. DHEW. Selected vital statistics for Indian Health 
Service Areas and Service Units, 1972-1977. DHEW Publication 
(HSA)79-1005. 

9. Health of Minorities and Women. Chartbook. American Public 
Health Association. Washington, D.C, 1982 

10. Health of the Disadvantaged. Chartbook II. September 1980 
DHHS Publication No. (HRA) 80-633. 

11. Kunitz SJ. Disease Change and the Role of Medicine. The 
Navajo Experience. University of California Press. Berkeley 
CA. 1983. 

12. Strotz CR, Shorr GI . Hypertension in the Papago Indians. 
Circ 1973;48:1299-1303. 

13. Howard BV, Lisse JR, Knowler WC, Davis MP, Pettitt DJ, 
Bennett PH. Diabetes and atherosclerosis in the Pima Indians. 
Mount Sinai J Med (NY) 1982;49:169-175. 



469 



14. Howard BV, Davis MP, Pettitt DJ, Knowler WC, Bennett PH. 
Plasma and lipoprotein cholesterol and triglceride concen- 
trations in the Pima Indians. Distributions differing from 
those of Caucasians. Circ 1983;68:714-724. 

15. Howard BV, Zech L, Davis M, Bennion LJ, Savage PJ, Nagulesparan 
M, Bilheimer D, Bennett PH, Grundy SM. Studies of very 

low density lipoprotein triglyceride metabolism in an obese 

population with low plasma lipids. Lack of influence of 

body weight or plasma insulin. J Lipid Res 1980;21:1032-1041. 

16. Reitman JS, Kosmakos FC, Howard BV, Taskinen MR, Kuusi 
T, Nikkila EA. Characterization of lipase activities in 
obese Pima Indians. J Clin Invest 1982;70:791-797. 

17. Savage PJ, Hamman RF, Bartha G, Dippe SE, Miller M, Bennett 
PH. Serum cholesterol levels in American (Pima) Indian 
children and adolescents. Pediatrics 1976;58:274-282. 

18. Klimes I, Nagulesparan M, Unger RH, Aronoff SL, Mott DM. 
Reduced Na+, K+ -ATPase activity in intact red cells and 
isolated membranes from obese man. J Clin Endocrinol Met 
1982;54:721-724. 

19. Nagulesparan M, Savage PJ, Mott DM, Johnson GJ, Unger RH, 
Bennett PH. Increased insulin resistance in obese, glucose- 
intolerant Southwestern American Indians. Evidence for 

a defect not explained by obesity . J Clin Endocrinol 
Met 1980;51:739-742. 

20. Pettitt DJ, Lisse JR, Knowler WC, Bennett PH. Mortality 

as a function of obesity and diabetes mellitus. Am J Epidemiol 
1982;115:359-366. 

21. Sasaki H, Nagulesparan M, Dubois A, Samloff M, Straus E, 
Sievers ML, Unger RH. Gastric function and obesity. Gastric 
emptying, gastric acid secretion, and plasma pepsinogen 

Int J Obesity 1984;8:183-190. 

22. Sievers ML. Cigarette and alchohol usage by Southwestern 
American Indians. Am J Pub Health 1968;58:77-82. 

23. Sievers ML. Myocardial infarction among Southwestern 
American Indians. Ann Int Med 1967;67:800-807. 

24. Garnick MB, Bennett PH, Langer T. Low density lipoprotein 
metabolism and lipoprotein cholesterol content in southwestern 
American Indians. J Lipid Res 1979;20:31-39. 

25. Keys A. Coronary heart disease--the global picture. 
Atherosclerosis 1975;22:149-192. 



470 



26. Clifford NJ, Kelly JJ, Leo TF, Eder HA. Coronary heart disease 
and hypertension in the White Mountain Apache tribe. Circ 
1963;28:926-931. 

27. DeStefano F, Coulehan JL, Wiant MK. Blood pressure survey 
on the Navajo Indian reservation. Am J Epidemiol 1979; 109: 
335-345. 

28. Leo TF, Kelly JJ, Eder HA. Cardiovascular survey in population 
of Arizona Indians. Circ 1958; 18: 748 (abstract). 

29. Sievers ML. Serum cholesterol levels in Southwestern 
American Indians. J Chron Dis 1968;21:107-115. 

30. Chase-the-Bear R, Bonnell M. Morse KG, Rate RG. Hopis 
and Navajos not lean. N Eng J Med 1979 ; 301: 1348 (letter). 

31. Fulmer HS, Roberts RW. Coronary heart disease among the 
Navajo Indians. Ann Int Med 1963;59:740-764. 

32. Connor WE, Cerqueira MT, Connor RW, Wallace RB, Malinow 

R, Casdorph HR. The plasma lipids, lipoproteins, and diet 
of the Tarahumara Indians of Mexico. Am J CLin Nutr 1978; 
31:1131-1142. 

33. Gillum RF, Gillum BS, Smith N. Cardiovascular risk factors 
among urban American Indians. Blood pressure, serum lipids, 
smoking, diabetes, health knowledge, and behavior. Am Heart 
J 1984;107:756-776 

34. Pinkerton RE, Badke FR. Coronary heart disease. An epidemi- 
ologic study of Crow and Northern Cheyenne Indians. Rocky 
Mount Med J 1974;71:577-583. 

35. Cockerham WC, Forslund MA, Raboin RM. Drug use among white 
and American Indian high school youth. Int J Addict 1976; 
11:209-220. 

36. Mayberry RH, Lindeman RD. A survey of chronic disease 
and diet in Seminole Indians in Oklahoma. Am J Clin Nutr 
1963;13:127-134. 

37. Porter MR, Vieira TA, Kaplan GJ, Heesch JR, Colyar AB . 
Drug use in Anchorage, Alaska. A survey of 15,634 students 
in grades 6 through 12-1971. JAMA 1973;223:657-664. 

38. Longclaws L, Barnes GE, Grieve L, Dumoff R. Alcohol and 
drug use among the Brokenhead Ojibwa. J Stud Alcohol 
1980;41:21-36. 



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39. Judkins RA. American Indian medicine and contemporary 
health problems. IV. Diabetes and perception of diabetes 
among Seneca Indians. NY State J Med 1978;78:1320-1323. 

40. Doeblin TD, Evans K, Ingall GB, Dowling K, Chilcote ME, 
Elsea W, Bannerman RM. Diabetes and hyperglycemia in Seneca 
Indians. Hum Hered 1969;19:613-627. 

41. Strimbu JL, Sims OS Jr. A university system drug profile. 
Int J Addict 1974;9:569-583. 

42. McMurry MP, Connor WE, Cerqueira MT. Dietary cholesterol 
and the plasma lipids and lipoproteins in the Tarahumara 
Indians --a People habituated to a low cholesterol diet 
after weaning. Am J Clin Nutr 1982;35:741-744. 

43. NCHS. Blood pressure levels of persons 6-74 years. United 
States, 1971-74, by Roberts J, Maurer K. Vital and Health 
Statistics. Series 11. No 203. DHEW Publication No. (HRA) 
78-1648. September 1977. 

44. U.S. DHEW. Indian Health Service. Sample Tribal-specific 
Comprehensive Health Plan. San Carlos Reservation. 1978. 

45. DHHS. Proceedings of the National Conference on High Blood 
Pressure Control in Native American Communities. NIH 
Publication No. 79-1960. April 1977 (reprinted August 1979) 

46. Ingelfinger JA, Bennett PH, Liebow IM, Miller M. Coronary 
heart disease in Pima Indians. Electrocardiographic findings 
and postmortem evidence of myocardial infarction in a population 
with a high prevalence of diabetes mellitus. Diabetes , 
1976;25:561-565. 

47. Sievers ML, Fisher JR. Increasing rate of acute myocardial 
infarction in southwestern American Indians . Ariz Med 
1979;36;739-742. (Cited in 3) 

48. Sievers ML. Historical overview of hypertension among 
American Indians and Alaskan Natives. Ariz. Med 1977; 
34:607-610. (cited in 3) 

49. Alfred BM. Blood pressure changes among male Navajo migrants 

to an urban environment. Canad Rev Soc Anthropol 1970;7:189-200. 
(cited in 33) . 

50. Scott Em, Griffith IV, Hoskins DD, Whaley RD. Serum cholesterol 
levels and blood pressures of Alaskan Eskimo men. Lancet 
1958;2:667-668. 



472 



51. Gillum RF, Prineas RJ, Palta M. , Horibe H. Blood pressures 
of urban Native American school children. Hypertension 
1980;2:744-749. 

52. Hamman RF, Bennett PH, Miller M. The effect of menopause 
on serum cholesterol in American (Pima) Indian women. 

Am J Epidemiol 1975;102:164-169. 

53. Thomas RK. The history of North American Indian alchohol 
use as a community-based phenomenon. J Studies Alcohol 
1981;suppl)9:29-39. 

54. Savage PJ, Dippe SE, Bennett PH, Gorden P, Roth J, Rushforth 
NB, Miller M. Hyperinsulinemia and hypoinsulinemia. Insulin 
responses to oral carbohydrate over a wide spectrum of 
glucose tolerance. Diabetes 1975;24:362-368. 

55. Sievers ML, Hendrix ME. Two weight-reduction programs 
among southwestern Indians. Health Serv Rep 1972;87:530-536. 

56. Westfall DN, Rosenblood AL. Diabetes mellitus among the 
Florida Seminoles . HSMHA Health Rep 1971;86:1037-1041. 

57. Reid JM, Fullmer SD, Pettigrew KD, Burch TA, Bennett PH, 
Miller M, Whedon GD. Nutrient intake of Pima Indian women. 
Relationships to diabetes mellitus and gallbladder disease. 
Am J' Clin Nutr 1971;24:1281-1289. 



473 



Stroke Report 





mi 



Lewis H. Kuller, M.D., Dr.P.H. 

Chairman, Department of Epidemiology 
Graduate School of Public Health 
University of Pittsburgh 
Pittsburgh, Pennsylvania 



MORTALITY 

Stroke is a major cause of death and disability in the United States. 
In 1981 there were 163,504 stroke deaths (Table 1), including 9,429 among 
non-white men and 11,310 non-white women. Most of these deaths, 8,760 
in men, and 10,656 were among black men and women. 

Age adjusted stroke death rates are approximately two times as high 
in the all other or black men and 1.8 times as high in black women than 
for white v. -(men who have the lowest death rates (Table 1). 

Age specific stroke death rates increase substantially with age 
(Table 2). Approximately doubling with each increase in 5 year age group 
(Table 2). Stroke death rates are much higher in the younger and middle 
aged blacks than whites (Table 2). The mortality rate is generally over 
3-fold higher through age 65 (Table 3). Stroke is estimated to reduce 
life expectancy at age 45 for non-white men by 12.3 years and for non- 
white women by 14.7 years (Manton and Baum, STROKE 1984;15:451-457). 

Stroke accounts for about seven percent of all deaths in 1981, 
including about 10% among black women (Table 4). Stroke is also an 
important contributing cause of death on the death certificate, that is 
not listed as the underlying cause (Table 5). 

In 1976-1978, the last year in which current data is available, 
stroke was the underlying cause for 31,368 deaths among black men and 
contributed to another 19,216 based on the death certificate listings 
and for women it was the underlying cause in 35,864 and in 21,313 a contri- 
buting cause. Previous studies have shown that when stroke is the under- 
lying cause of death, the individual has usually died from the acute 
complications of stroke usually within the first several months after 
the stroke. However, many other individuals who survive the initial 
stroke event may subsequently die of a stroke or related cause without 
any mention of this on the death certificate. i 

There is a very substantial variation in stroke mortality by 
geographic area. These differences have persisted for many years. In 
1969-1971 (Table 6), stroke death rates were 10 times higher for black 
men in Savannah, Georgia than for white men in Baltimore, Maryland aged 
45-54. In 1978 stroke death rates aged 45-54 were still four times higher 
in Georgia for black men than for white men and 3.5 times higher for 
black than white women. Rates were still substantially higher in Georgia 
and other areas of the southeast than in the Great Plains or Rocky Mountain 
areas (Tables 7 ?-nd 8). 

Previous studies have clearly demonstrated a marked socioeconomic 
gradient in stroke mortality for both black men and women (Table 9). 
There are also marked variations in stroke mortality within a state such 
as North Carolina (Table 10). A recent study in Allegheny County, 
Pennsylvania, for white men continues to demonstrate a considerable socio- 
economic gradient in stroke mortality. These observations are consistent 
with a greater prevalence of risk factors especially hypertension in 
lower socioeconomic and less educated populations and also poor control 
of these risk factors. 



477 



High stroke death rates among blacks are not limited to the United 
States. Stroke is reported to be increasing and common in Africa. A 
recent WHO report noted stroke rates in Cape Verde Islands (Table 11), 
similar to those of blacks in the United States. Unfortunately mortality 
statistics for other countries in Africa with predominantly black 
populations are not available. However, clinical studies suggest an 
increase stroke mortality associated with hypertension especially in 
urban areas. In the March, 1983 report of the East Africa Medical Journal, 
Daresi, et al., noted that cerebral vascular disease was becoming a major 
cause of mortality and morbidity. One hundred eighty stroke cases and 
180 age and sex matched controls were studies over a two year period in 
Lagos, Nigeria. The stroke patients had a much higher prevalence of 
systolic and diastolic hypertension, diabetes mellitus and obesity. 

In Lagos University Teaching Hospital, cerebrovascular accidents 
were the second most common of all neurological admissions between 1962 
and 1967, the most common being tetanus. Evidence from the Stroke Registry 
in Ibadan, Nigeria, has shown that the incidence of stroke was 26/100,000. 
Daresi, et. al.. East Africa Medical Journal, March 1983. 

The prevalence of cerebro atherosclerosis increases in Nigeria with 
age and with the presence of a history of hypertension (Table 12). The 
prevalence is not as high as in U.S. populations (Table 12). Therefore, 
the current evidence from Africa suggest that stroke is becoming 
increasingly prevalent, that it is related to hypertension and perhaps 
diabetes, and that cerebral atherosclerotic disease is increasing especially 
among hypertensives. Coronary artery disease and myocardial infarction 
is still very uncommon. The picture in Africa especially in urban west 
Africa is probably a replication of changes in risk factors and stroke 
that occurred many years ago in the United States. 

Blacks in the United States are also reported to have a higher 
prevalence of both intracranial and extracranial pathology as compared 
to whites (Tables 13-14). 

Stroke death rates are not elevated among the Chinese, Japanese, 
Koreans and Philippino's compared with U.S. whites in the United States 
(Tables 15-17). There also does not appear to be an excess stroke 
mortality among Hispanics in Southern Texas (Table 18) as compared to 
whites. There may be a slight excess of stroke mortality among Puerto 
Ricans in New York especially in the younger age groups as compared to 
whites (Table 19). The apparent absence of an increase in stroke death 
rates among Mexican-American populations may be of particular importance. 
This population is generally of lower socioeconomic status, has a very 
high prevalence of obesity especially among women, and diabetes, but 
little increase in hypertension. The failure to note an apparent increase 
in hypertension with acculturation may be due to genetic factors or diet. 
Further investigation of this population should be done especially in 
search of possible protective constituents in the diet or selected genetic 
factors. 

Stroke death rates among American Indians appear to be slightly 
higher than the rest of the United States population, but lower than 
those for U.S. blacks. Stroke death rates also appear to be declining 
among American Indians (Tables 20-21). 



478 



The substantial epidemic of stroke mortality among minorities appears 
to be predominantly limited to the United States blacks, especially those 
in the southeast and probably in the lower socioeconomic groups. 

Stroke death rates for blacks and whites are decreasing. This 
decrease has been noted since the 1920 's (Table 22-23). The decrease in 
stroke mortality has been accentuated in recent years (Table 24) and 
affects all age groups. The decline has been greater for black women 
(Table 25). The decline has also been greater for cerebral hemorrhage 
than thrombosis. However, the accuracy of specific type of stroke 
diagnosis on the death certificate is suspect. 

The decline in stroke mortality began prior to the introduction of 
drug treatment for hypertension. The decline paralleled a similar overall 
decrease in cardiovascular-renal mortality and was inversely related to 
the increase in heart disease death rates especially among men. A re- 
coding of the death certificates was done in the Baltimore and Memphis 
study, (Table 23), and probably rules out any changes in certification 
practices in filling out death certificates as the reasons for this decline. 
The accuracy of the diagnosis may remain suspect especially for deaths 
outside of the hospital and in the older age groups. More detailed studies 
from Rochester, Minnesota, with careful evaluation of the accuracy of 
the diagnoses, suggest the decline in the incidence of stroke especially 
among women beginning at least in the early 1940 's (Table 26). The 
determinants of the decline in stroke over time may be similar to the 
model previously noted for tuberculosis. Much of the decline in 
tuberculosis occurred prior to the introduction of specific drug therapy. 
This may be the same case with regard to stroke and the introduction of 
hypertensive drug therapy. There was then a secondary accentuation of 
the decrease following the introduction of specific therapy both for 
tuberculosis and for the treatment of hypertension and prevention of 
stroke. The reasons for the non-specific decline prior to the introduction 
of specific drug therapy is unknown but may be related to diet or reduction 
of renal disease, secondary to infection. 

The decline in stroke mortality has occurred in both the high and 
low death rate areas of the United States (Tables 27-28). A similar 
decline in stroke mortality has occurred in other countries (Table 29). 
The decline in stroke mortality in other minority groups in the United 
States is less well documented. Stroke mortality has declined among the 
Hispanics in San Antonio, probably among the Japanese in Hawaii and among 
American Indians (see previous tables). The decline has resulted in 
some narrowing of the geographic variations in stroke mortality in the 
United States (Table 27). The decline in stroke death rates between 
1970-1980 are similar for blacks and whites, and for age groups 35-84 
(Table 30). There is no current data that demonstrates whether the stroke 
death rates are declining faster in communities with specific hypertension 
control programs as compared to the rest of the country. Such detailed 
information is badly needed in order to evaluate the impact of these 
intensive programs. The decline in stroke death rates appears to be 
similar in the United States and several other countries (Table 31), 
however, in many of these countries there has also been a vigorous attempt 
to treat hypertensive disease. The exception may be Taiwan in which the 
death rates have declined inspite of the absence of an extensive treatment 
program. 



479 



MORBIDITY 

Information pertaining to stroke morbidity as compared to mortality 
is more difficult to identify especially as related to specific minority 
groups. The 1972 National Health Interview Survey estimated the prevalence 
of stroke as 7.2/1,000 among whites and 9.1/1,000 among all others. 

The prevalence of stroke reported in the Evans County, Georgia study 
in 1967-1969 was 53.2/1,000 for white males, 15.0 for white women, 58.6 
for black men and 43.4 for black women age adjusted (Table 32). 

Among participants eligible for randomization in the Hypertension 
Detection and Prevention Trial, the prevalence of stroke was much higher 
in blacks than whites. 

The data on the prevalence of stroke among whites has been provided 
by previous national stroke surveys, but no data for blacks was included 
in that report or for other minority groups. The need for including 
larger numbers of minorities in future prevalence surveys is obvious if 
good prevalence data is to be obtained. 

The prevalence of stroke among Japanese in Hawaii and California 
was much lower than for Japanese in Japan (Table 33). 

There were 806,000 stroke hospital discharges in which stroke was 
the first listed diagnosis in 1981 in the United States including 100,000 
among non-whites (Table 34). The average length of stay was slightly - 
longer for other racial groups than for whites. Based on these data, 
there were approximately 1.4 million hospital days directly related to 
stroke care among non-whites. 

The estimated annual medical care cost of stroke in 1980 was 5.1 
billion dollars, half of which was for hospital care. Non-whites accounted 
for about 1/8 of the hospital days or a minimum of 300 million dollars 
for their hospital care alone. The total cost of stroke care for both 
whites and non-whites in the United States is very substantial (Table 
35). 

Data on the incidence of stroke among several minority groups is 
available. The southern Alabama study is the most recent and most complete 
(Table 36). The age adjusted incidence is higher in blacks than whites 
especially for black women. 

The risk of stroke was also substantially higher among black men 
and women in the Hypertension Detection and Follow-up Program clinical 
trial for both the stepped and referred care populations (Table 37). 

Stroke incidence has also been measured among blacks in Ibadan, 
Nigeria (Table 38). Stroke rates in Ibadan appear to be in the same 
range as those noted in the southern Alabama study. For example, age 
specific incidence per 100,000 in Ibadan, ages 50-59, is 440/100,000 as 
compared to a rate of 642/100,000 aged 55-64 in southern Alabama. It is 
unclear however, whether the Ibadan rates are from one or three years. 
It is also unclear what percentage of stroke cases are actually ascertained 



480 



in Ibadan as compared to the southern Alabama study. The high stroke 
incidence rates may not be limited to the U.S. black population. 

Stroke incidence is comparable among Japanese living in Hawaii and 
the U.S. white population. Stroke incidence is much lower among the 
Japanese in Hawaii than for the Japanese in Japan (Table 39). There is 
no evidence for increased stroke death rates among Chinese in the United 
States. Chinese in Taiwan have the highest stroke death rates reported 
(Table 31). Stroke death rates are declining in Taiwan even though there 
is no apparent well-organized hypertension control program (Table 31). 
Prophylactic approaches to hypertensive diseases (Y. Yamori, Raven Press, 
New York 1979). A stroke registry in part of Taipei in 1975 reported a 
stroke incidence rate aged 55-64 substantially higher than in the United 
States whites, 11.6/100,000 in men, as compared to 2.7/100,000 in Southern 
Alabama (Table 40) . The remarkable apparent decrease in stroke among 
both Chinese and Japanese migrants to the United States certainly requires 
further evaluation especially as it does not appear to be directly related 
to changes in blood pressure levels. 

Stroke is not a single disease but rather a group of related 
diagnoses. Many investigators believe that blacks and Japanese have 
more intracranial and more hemorrhagic disease than whites. Few studies 
have documented the specific types of stroke based on good clinical and 
laboratory-diagnostic evaluations . 

The stroke study in Southern Alabama included a detailed review of 
the specific types of stroke based on careful clinical evaluations. Most 
strokes in both blacks and whites were due to infarction rather than 
hemorrhage (Table 41). Thromboembolic stroke also predominants among 
Japanese in Japan as well as among Japanese in Hawaii (Tables 42-43). 
Further evaluation of the specific types of strokes will be possible 
with the development of new technology for evaluating stroke diagnosis 
such as CT scan and NMR, etc. The availability of improved diagnostic 
methods may provide a better understanding of the interrelationship of 
some of the key risk factors for stroke especially the relationships if 
any between the types of hypertensive disease and specific clinical- 
pathology of stroke. 



RISK FACTORS 

Hypertension is the major risk factor for stroke. Diabetes, alcohol 
intake, high hematocrit or hemoglobin and lipoprotein abnormalities may 
also be important risk factors. 

Other cardiovascular disease, specific electrocardiographic 
abnormalities especially signs of left ventricular hypertrophy, as well 
as other manifestations of increased left ventricular mass such as an 
increased left ventricular wall mass by echocardiography and cardiac 
arrhythmias including atrial fibrillation are major risk factors for 
stroke. 

Both systolic and diastolic blood pressures are higher in blacks 
than whites (Table 44). 



481 



The prevalence of elevated blood pressure increases substantially 
with increasing age among both blacks and whites (Table 45). The decline 
in the prevalence of elevated blood pressure, as noted in Table 45, is 
apparently primarily due to the treatment of hypertension which has 
substantially improved over time. 

Blood pressure increased with age among Mexican Americans. Blood 
pressure levels appear to be similar among Mexican American and U.S. 
whites (Table 46). 

Blood pressure among American Indians in Minnesota were similar to 
those of U.S. whites (Table 47). No data could be obtained on the blood 
pressure distribution of Indians living on the reservations in the south- 
western United States. 

Blood pressures are higher among Japanese in the United States than 
among Japanese in Japan (Table 48). This is surprising because of the 
much higher stroke death rates among Japanese in Japan than those in the 
United States. The blood pressures of Japanese in Hawaii and California 
are similar to those of the U.S. whites. Part of the difference in blood 
pressure between Japanese in Japan and Hawaii may be related to a greater 
prevalence of obesity among U.S. Japanese. However, obesity adjusted 
blood pressures are either similar or slightly higher among U.S. Japanese 
than those in Japan (Table 49). Similar studies of blood pressure 
distribution of Chinese in Taiwan fail to demonstrate any higher levels 
as compared to other populations inspite of the much higher stroke death 
rates (Table 50). 

The prevalence of hypertension is also higher among Japanese in the 
United States (Table 51). The prevalence of electrocardiographic evidence 
of left ventricular hypertrophy and hypertensive heart disease is however 
much higher among Japanese in Japan than in Hawaii or California (Table 
52). This is also true even when comparing electrocardiographic 
abnormalities among Japanese in Japan working for the NTT Telephone 
Company versus U.S. telephone workers (Table 53). There is also a 
relationship between the high R-waves on the electrocardiograph and 
elevated blood pressure in both of these populations. There is evidence 
from studies both in Japan and in Hawaii that these electrocardiographic 
abnormalities may be an independent predictor of stroke incidence and 
mortality. The higher prevalence of left ventricular hypertrophy in 
relationship to hypertension has been noted in Chinese in Taiwan (see 
ref. Fig. 50). 

The prevalence of electrocardiographic abnormalities was also noted 
to be much higher among blacks even after controlling for the degree of 
hypertension. This has been noted most recently in both the Multiple 
Risk Factor Intervention Trial (MRFIT) (Table 54) and the Hypertension 
Detection and Follow-up Program (HDFP). 

There have been numerous surveys of selected population groups in 
Africa. Few of the studies represent true population samples or comparable 
methods of measurement. The studies were reviewed by Adenounmu (Clinical 
and Experimental Hypertension, 1981;3(4) :597-621) . He noted that blood 
pressure increases with age and is higher in urban than rural men in 



482 



I 



Africa (Table 55). The blood pressure levels are similar to those in 
the Carribean Islands but lower than in the U.S. or south Africian blacks. 
Stroke, congestive heart failure and renal diseases are the major 
complications of hypertension. Coronary artery disease remains very 
rare. 

Earlier studies such as from Evans County, Georgia (Table 56) suggested 
relatively little difference in the risk of stroke in relationship to 
blood pressure level among blacks and whites. More recent studies, however, 
suggest that black hypertensives may be at greater risk of stroke than 
white hypertensives. The estimated incidence of stroke in the referred 
care group for blacks in the Hypertension Detection and Follow-up Program 
was 35.3/1,000 as compared to 24.2/1,000 for whites. There was a 
substantial decrease in stroke morbidity and mortality in the special 
care as compared to the referred care for all four race, sex groups (Table 
57). 

In the Multiple Risk Factor Intervention Trial the ineligible 
screenees were followed initially for five years. Among the screenees 
there were 23,490, black men between the ages of 35-57. The incidence 
of stroke, was 1.3/1,000 among black men and 0.5/1,000 for white men 
(Table 58). The risk of stroke death increased with level of diastolic 
blood pressure (Table 59). At most, levels of diastolic blood pressure 
the stroke rates were higher in blacks than whites. 

The logistic regression coefficient for the risk of stroke death 
was greater for black men than white men (Table 60) suggesting that at a 
given level of blood pressure the risk of stroke death is greater for 
blacks than whites. However, part of this difference could be due to 
differential subsequent treatment for hypertension. 

The risk of stroke was increased among individuals with electro- 
cardiographic abnormalities in the Evans County Study, this was true for 
all four race/sex groups but especially for men (Table 61). In the HDFP 
trial the mortality rates including stroke were increased among men with 
electrocardiographic abnormalities based on the "Minnesota Code" (Table 
62-63). 

Stroke incidence is also directly related to blood pressure levels 
among Japanese men in Hawaii (Table 64). The increased risk appears to 
be related to both intracranial hemorrhage and thromboembolic disease 
(Table 64). It appears that at higher levels of systolic blood pressure 
the Japanese in Japan have a greater risk of stroke than Japanese in 
Hawaii (Table 65). 

Surveys in Taipai also demonstrate a striking association between 
hypertension and stroke, as well as the high prevalence of left ventricular 
hypertrophy (Table 66). 

The relationship between lipoprotein levels and risk of stroke is 
equivocal. In the Evans County Study there was no consistent relationship 
between the serum cholesterol level and risk of stroke among blacks or 
whites (Table 67). 



483 



In the MRFIT screenees there was also no consistent relationship 
between the serum cholesterol level and risk of stroke death for either 
black or white men (Table 68). None of the regression coefficients related 
to serum cholesterol and risk of stroke were significant (Table 69). 

Prior studies in Japan had suggested a possible inverse relationship 
between stroke and serum cholesterol levels. Studies of Japanese in 
Hawaii are consistent in demonstrating a possible inverse relationship 
between serum cholesterol levels and cerebral hemorrhage but not for 
cerebral thrombosis or infarction (Table 70). 

More recent studies from Japan (Table 71) do not demonstrate a 
consistent relationship between the serum cholesterol level and stroke 
except for a lower cholesterol levels among the small number of individuals 
with cerebral hemorrhage. These initial studies however do demonstrate 
that lower animal protein and very low saturated fat intake may be a 
risk factor for stroke (Tables 72-73). 

A further analysis of the Japanese in Hawaii based on post-mortem 
measurement of cerebrovascular disease again demonstrated a slightly 
lower cholesterol level among deaths with cerebral hemorrhage and higher 
cholesterol for those found with a brain infarction. Animal protein 
intake was decreased only for deaths with cerebral hemorrhage. 

This data set further demonstrated a relationship between cerebral 
and aortic atherosclerosis and brain infarction and also a high prevalence 
of prior myocardial infarction among those also found to have brain 
infarction by post-mortem examination (Tables 73-74). The results of 
these studies therefore suggest that the relationship between lipoproteins, 
dietary factors and stroke may be different for those who have cerebral 
thromboembolic disease as compared to cerebral hemorrhage. 

Cerebral thromboembolic disease secondary to atherosclerosis is by 
far the most common stroke disorder in the U.S. black and white population 
as well as among the Japanese in Hawaii and California. The primary 
emphasis should obviously be placed on the risk factors for this disorder. 
On the other hand, the relationships between low protein intake and 
cerebral hemorrhage especially animal protein may be a clue to the 
apparent sharp decline in cerebral hemorrhage over the past 20 and 30 
years associated with improved diet and lifestyle including a probable 
increase in animal protein intake. 

The prevalence of diabetes is also substantially higher among blacks 
as compared to whites (Table 75). Diabetes is also very prevalent among 
several American Indian tribes and among Mexican Americans in the 
southwestern United States. 

Diabetes is an important risk factor for stroke. Blacks have a 
higher prevalence of diabetes than whites. In the Three-Area Study of 
Stroke Risk Factors, blacks had higher blood sugars and history of diabetes 
than whites especially in the southeastern United States (Table 76). 
Diabetes is clearly associated with an increase in cerebro atherosclerosis 
(Table 77). Prospective studies such as the American Cancer Society 
Followup Study, (Table 78) or the Framingham Study (Table 79) have noted 
the increase risk of stroke among diabetics. 

484 



i 



A study in the 1960's demonstrated that diabetes was a frequent 
contributing cause of death on a death certificate in which stroke was 
the underlying cause especially among black women (Table 80). Studies 
in the late 1960's (Table 81) showed that diabetes was listed on about 
16% of all stroke hospital discharges. A more recent, unpublished study, 
from Pennsylvania showed that stroke was listed as a secondary diagnosis 
on 2.7% of hospital discharges for diabetes among blacks and 4.8% among 
whites, and in 5.2% of the records among blacks when diabetes was listed 
as a secondary diagnosis on the hospital discharge record. 

A followup study of a diabetic cohort in Rochester, Minnesota 
suggested that the increased risk of stroke among diabetics may be limited 
to those with concurrent hypertension (Table 82). This observation could 
explain the lower rates of stroke inspite of the high prevalence of 
diabetes among Hispanics and Mexican Americans due to their apparent 
lower prevalence of hypertension as compared to U.S. blacks. 

The prospective Honolulu Heart Study has further documented an 
increased risk of stroke especially thromboembolic associated with 
increasing levels of blood sugar (Table 83). In multivariate analysis, 
the blood sugar levels remained an independent predictor of thromboembolic 
stroke but not hemorrhage. 



OTHER RISK FACTORS 

Alcohol Consumption 

Alcohol consumption has been identified as an independent predictor 
of stroke as well as a possible risk factor for elevated blood pressure. 
Among Japanese in Hawaii, there was a direct relationship between alcohol 
consumption and cerebral hemorrhage but not cerebral thrombosis (Table 
84, 85). Alcohol consumption and hypertension may be an especially lethal 
combination for cerebral hemorrhage. A major effort must be made to 
treat hypertension among alcohol consumers, as well as reducing prevalence 
of alcoholism. 



Cigarette Smoking 

The relationship between cigarette smoking and stroke is uncertain. 
Among Japanese in Hawaii, there was a statistically non-significant greater 
number of cigarettes smoked among subsequent cerebral hemorrhage or thrombosis 
cases than non-strokes. In the MRFIT trial screenees, the risk of stroke 
appeared to increase up to 26-35 cigarettes per day and then decrease 
among black men (Table 86). Cigarette smoking has an important effect 
on platelets and thrombogenesis. It is possible that smoking could be 
an important precipitant of stroke among individuals with a high risk of 
cerebro thromboembolism especially those with carotid artery stenosis, 
heart disease and cardiac arrhythmias. 



485 



Hematocrit and Hemoglobin 

Many studies such as the "Framingham Heart Study", have shown a 
direct relationship between hematocrit or hemoglobin levels and risk of 
stroke. The relationship may be due to an association of elevated hemo- 
globin or hematocrit with blood pressure to greater viscosity of the 
blood or to other unknown pathophysiological changes associated with the 
level of hematocrit or hemoglobin. In the Evans County Study, there 
appeared to be an increased risk of stroke among both blacks and whites 
with increasing hematocrit levels (Table 87). These studies may have 
important implications for defining ideal hematocrit or hemoglobin levels 
especially among women. It is possible that the lower levels of hemoglobin 
or hematocrit in women secondary to recurrent menstrual bleeding offer 
some protection against thromboembolic disease. Attempts to raise these 
levels could increase the risk of stroke or other thromboembolic diseases. 

Sickle cell anemia is an important cause of stroke especially in 
the younger age groups. There is no evidence however that sickle cell 
trait or other hemoglobin disorders are associated with a substantial 
increased risk of stroke. 



COMBINATION OF RISK FACTORS 

A combination of these risk factors such as in the Hawaii Heart 
Study of Japanese men (Table 88) can identify a high risk of stroke. 
The combination of several of these risk factors plus hypertension (Tahle 
88) defines a much higher risk group. Many of these risk factors are 
clearly ameanable to preventive efforts. 



DISCUSSION AND IMPLICATIONS 

The death rates due to stroke have continued their long-term decline. 
The slope of the decline accentuated in the mid 1970' s most likely due 
to an improvement in the treatment and control of hypertension. The 
changes in awareness, treatment and control of hypertension as noted in 
the "Impact Study" (Table 89) have resulted in a decrease in the 
prevalence of elevated diastolic blood pressure. Blood pressure remains 
substantially higher among blacks than whites. Improvement in the control 
of hypertension has also occurred among Mexican Americans (Table 90) and 
probably among Japanese and other minority groups in Hawaii and California. 

Inspite of these good efforts the stroke death rates and incidence 
still remain much higher among blacks than whites. There is little 
evidence that other minority groups such as Hispanics, Chinese, Japanese, 
Koreans or native Americans are at substantially higher risk of stroke 
than whites. The risk may be elevated among Puerto Ricans in New York. 
No data could be obtained for Cubans in the southeast or for Vietnamese 
or other Asian groups. 

The risks of stroke are related primarily to hypertension. Prevention 
and treatment of hypertension remains the cornerstone of any stroke control 
program. The increased prevalence of hypertension among blacks is probably 



486 



a combination of genetic and environmental factors. Clinical and 
epidemiological studies have identified differences in renin, sodium, 
lithium counter transport, the ability to excrete a salt load and urinary 
kallikrein excretion between blacks and whites. Elevated blood pressure 
is clearly not due to any one single factor. The type of blood pressure 
elevation and relationship to outcome may vary in relationship to the 
key risk factors. 

Obesity is the most important risk factor for elevated blood pressure 
in the United States. However, obesity related hypertension may be a 
different type of disease than non-obesity hypertension especially in 
relation to specific hypertensive outcomes, such as, cerebral hemorrhage, 
intracranial vascular disease, renal disease, and retinopathy. Obesity 
hypertension may be a more important factor for atherosclerotic disease 
including myocardial infarction. The decline in stroke that occurred 
from the 1920 's and 1930 's may be related to this non-obesity related 
hypertension. A recent report from the Hypertension Detection and 
Followup Program noted a substantially higher mortality among those with 
non-obese, as compared to obesity hypertension (Table 91). Other 
hypertensive studies have shown similar results. 

The origins of non-obesity hypertension is unknown but low protein 
intake, high intake of salt and low consumption of potassium and calcium 
may be playing important roles. There is also most likely an important 
genetic component. It is important to reiterate that both obese and 
non-obese hypertension must be treated in order to reduce the specific 
hypertensive complications especially stroke. The lower the blood pressure 
the greater the decrease in hypertensive complications especially stroke 
and congestive heart failure. The only issue perhaps that still remains 
is the interaction between the treatment of hypertension and atherosclerotic 
complications especially myocardial infarction. 

The highest rates of hypertension and stroke among blacks are found 
in the southeast, in lower socioeconomic groups and among less educated 
individuals. Key environmental factors appear to play an important role 
in these geographic and socioeconomic variations including obesity, sodium, 
potassium, and calcium intake, possibly stress and "hostility", alcohol 
intake and health care especially as related to the treatment of 
hypertension and its complications. 

The control of diabetes and hypertension especially the combination 
of diabetes and hypertension among black women may be associated with an 
exceptionally high risk of stroke. The joint prevalence of hypertension 
and diabetes may both be primarily related to nutritional factors especially 
the development of obesity. 

The future accentuation of the rapid reduction of stroke mortality 
and morbidity especially among blacks will require efforts focused at 
identifying the high risk individuals and communities in the United States, 
and aggressive control of hypertension and other risk factors in these 
high risk communities. Such communities can be easily identified by 
monitoring the high stroke death rates. Such communities should be candidates 
for aggressive hypertension treatment programs and careful monitoring to 
determine a consistent reduction in stroke mortality. The stroke death 



487 



rates in general reflect the acute stroke case fatality which is generally 
at least 20-30%. Mortality rates reflect the trends in the incidence of 
stroke and are the easiest and best endpoint to monitor in hypertension 
control programs. The reduction in stroke mortality especially among 
younger blacks, i.e., 35-64, is probably the most important medical factor 
in decreasing the black-white difference in mortality rates among adults. 

Major efforts should be continued to reduce the prevalence of elevated 
blood pressure by control of risk factors for hypertension. The ultimate 
control of this epidemic of hypertension and stroke will depend on primary 
prevention. Much of the health habits which lead to the elevated risk 
factors are learned early in life and therefore may be ameanable to modifi- 
cation. Nutrition and genetic factors are probably the key elements. 

The role of diabetes and hyperlipoproteinemia in the etiology of 
stroke especially among blacks needs further investigation. It is unclear 
whether elevated levels of HDL cholesterol or its subfractions are associated 
with a reduced risk of stroke especially thromboembolic stroke as well 
as heart attack. There is little evidence that treatment of non-insulin 
dependent diabetes with either oral hypoglycemic agents or insulin reduces 
the risk of stroke. There is a strong genetic component to diabetes, as 
well as a clear relationship to dietary factors especially obesity and 
perhaps a low fiber intake. Prevention of diabetes and a better 
understanding of its pathophysiology and improved methods of treatment 
offer the best potential for the prevention of the complications of this 
disease including stroke. 

Treatment of stroke may have improved in recent years. There is 
some evidence for reduction in the case fatality. Diagnostic methods 
have certainly improved substantially. Early detection and treatment of 
potential strokes may be of substantial value especially the identification 
of transient ischemic attacks and the possible treatment with antiplatelet 
agents or surgical correction of underlying carotid artery disease or 
identification of carotid artery bruit and asymptomatic stenosis and 
occlusion. 

There is also a strong association between vascular disease at other 
sites especially coronary artery disease and subsequent risk of stroke. 

Patients who have had a myocardial infarctions or other manifestations 
of coronary artery disease are ideal candidates for preventive efforts 
to reduce the subsequent risk of stroke. Furthermore, there appears to 
be a strong association between certain electrocardiographic and 
echocardiographic abnormalities, and subsequent risk of stroke. The 
identification of such high risk individuals and effective treatment may 
also be important in reducing the risk of stroke. There is strong evidence 
that blacks, as well as Japanese may have more intracranial and less 
extracranial disease than whites (Tables 92-93) and therefore such approaches 
as carotid artery surgery, antiplatelet drugs may be less effective in 
black populations. The major effort to reduce stroke mortality should 
continue to emphasize identification, treatment and control of hypertension. 
The risk factors for stroke are identifiable and can be controlled effectively. 



I 



488 



TABLE 1 



Age Adjusted Death Rates Due to Cerebrovascular 
Disease (430-438) 1981— United States by Race and Sex 



Total 
Men 
Women 
White Men 
White Women 
All Other Men 
All Other Women 
Black Men 
Black Women 







Ratio to 


Number of Deaths 


Rate/ 100, 000 


White Women 


163,504 


38.1 


1.1 


66,429 


41.7 


1.3 


97,075 


35.4 


1.1 


57,000 


38.9 


1.2 


85,765 


33.1 


1 


9,429 


65.6 


2.0 


11,310 


53.2 


1.6 


8,760 


72.7 


2.2 


10,656 


58.1 


1.8 



Monthly Vital Statistics Reports. National Center for 
Health Statistics, Vol. 33, No. 3, Supplement, June, 1984. 



489 



TABLE 2 



Death rates for cerebrovascular diseases, according to race, sex, and age: United States, 

selected years 1950-82 



(Data are based on the National Vital Statistics System) 



Race, sex, and age 



1950' 



Year 



I960' 



1970 



1975 



1979 



1980 



198r 



1982' 



Total-^ 

4 

All ages, age adjusted 88.8 

All ages, crude 104.0 

Under 1 year 5.1 

1-4 years 0.9 

5-14 years 0.5 

15-24 years 1.6 

25-34 years 4.2 

35-44 years 18.7 

45-54 years 70.4 

55-64 years 195.3 

65-74 years 549.7 

75-84 years 1,499.6 

85 years and over 2,990.1 



Number of deaths per 100,000 resident population 



79.7 


66.3 


53.7 


41.6 


40.8 


38.3 


36.1 


108.0 


101.9 


90.1 


75.5 


75.1 


71.3 


68.9 


4.1 


5.0 


5.0 


4.6 


4.4 


3.6 


3.8 


0.8 
0,7 


1.0 
0.7 


0.8 
0.5 


0.3 
0.3 


0.5> 
0.3» 


0.2 


0.2 


1.8 


1.6 


1.4 


0.9 


1.0 


0.9 


1.0 


4.7 


4.5 


3.4 


2.6 


2.6 


2.6 


2.3 


14.7 


15.6 


11.7 


9.1 


8.5 


8.1 


7.9 


49.2 


41.6 


32.3 


26.4 


25.2 


26.3 


24.2 


147.3 


115.8 


90.4 


68.1 


65.2 


64.5 


57.2 


469.2 


384.1 


302.2 


226.9 


219.5 


209.8 


195.3 


491.3 


1,254.2 


1,028.8 


793.8 


788.6 


702.6 


678.6 


680.5 


3,234.6 


2,736.4 


2,264.9 


2,288.9 


2,119.8 


2,056.4 



White male 

4 

All ages, age adjusted 87.0 

All ages, crude 100.5 

Under 1 year 5.9 

1-4 years 1.1 

5-14 years 0.5 

15-24 years 1.6 

25-34 years 3.4 

35-44 years 13.1 

45-54 years 53.7 

55-64 years 182.2 

65-74 years 569.7 

75-84 years 1,556.3 

85 years and over 3,127.1 



80.3 


68.8 


56.7 


42.9 


41.9 


102.7 


93.5 


80.2 


64.2 


63.3 


4.3 


4.5 


4.6 


3.6 


3.8 


0.8 


1.2 


0.9 


0.3 


0.4 


0.7 


0.8 


0.5 


0.3 


0.2 


1.7 


1.6 


1.4 


0.9 


1.0 


3.5 


3.2 


2.6 


2.2 


2.0 


11.3 


11.8 


8.7 


6.8 


6.5 


40.9 


35.6 


27.6 


22.2 


21.7 


139.0 


119.9 


93.8 


68.0 


64.2 


501.0 


420.0 


339.4 


249.5 


240.4 


1,564.8 


1,361.6 


1,134.9 


867.0 


854.8 


3.734.8 


3,317.6 


2.807.4 


2,224.5 


2.236.9 



White female 

4 

All ages, age adjusted 79.7 

All ages, crude 103.3 

Under 1 year 2.9 

1-4 years 0.6 

5-14 years 0.4 

15-24 years 1.2 

25-34 years 2.9 

35-44 years 13.6 

45-54 years 55.0 

55-64 years 156.9 

65-74 years 198.1 

75-84 years 1.471.3 

85 years and over 3,017.9 

See footnotes at end of table. 



68.7 


56.2 


46.1 


35.9 


35.2 


110.1 


109.8 


101.6 


88.5 


88.8 


2.6 


3.2 


3.9 


3.3 


3.3 


0.5 


0.6 


0.7 


0.3 


0.4 


0.6 


0.6 


.0.5 


0.3 


0.3 


1.4 


1.1 


1.1 


0.7 


0.7 


3.4 


3.4 


3.0 


2.0 


2.0 


10.1 


11.5 


9.3 


7.0 


6.7 


33.8 


30.5 


25.0 


20.1 


18.7 


103.0 


78.1 


64.5 


50.6 


48.7 


383.3 


303.2 


233.6 


179.2 


172.8 


1,444.7 


1,176.8 


966.2 


739.3 


730.3 


3,795.7 


3,316.1 


2.794.9 


2.335.7 


2.367.8 



Health-United States, 1983. 



490 



TABLE 2 (cont.) 



Death rates fqr cerebrovascular diseases, according to race, sex, and age: United States, 
selected years 1950-82--Continued 

(Data are based on the National Vital Statistics System) 



Race, sex, and age 



1950"^ 



Year 



1960^ 



1970 



1975 



1979 



1980 



198r 



1982' 



Black male 

4 

All ages, age adjusted 

All ages, crude 

Under 1 year 

1-4 years I 

5-14 years 

15-24 years 

25-34 years 

35-44 years 

45-54 years 

55-64 years 

65-74 years 

75-84 years 

85 years and over { 



Number of deaths per 100,000 resident population 



146.2 


141.2 


124.2 


95.0 


77.9 


77.5 


122.0 


122.9 


108.7 


87.8 


73.8 


73.1 


2.5 


8.5 


12.2 


9.1 


12.7 


11.2 


1.9 


•1.4 


1.1 


0.5 


0.6 


0.7 


•0.9 


0.8 


0.7 


0.3 


0.5 


3.3 


3.7 


3.0 


2.5 


1.4 


2.1 


12.0 


12.8 


14.6 


9.4 


7.3 


7.7 


59.3 


47.4 


52.7 


36.9 


34.4 


29.2 


211.9 


166.1 


136.2 


98.0 


88.8 


82.1 


522.8 


439.9 


343.4 


253.7 


204.0 


189.8 


783.6 


899.2 


780.0 


626.9 


470.9 


472.8 


504.9 


1,475.2 


1,442.6 


1,123.0 


963.9 


1,067.6 


2,700.0 


2,315.4 


2,115.2 


1,840.4 


1,873.2 



Black female 

4 

All ages, age adjusted 

All ages, crude 

Under 1 year > 

1-4 years { 

5-14 years 

15-24 years 

25-34 years 

35-44 years 

45-54 years 

55-64 years 

65-74 years 

75-84 years i 

85 years and over i 



155.6 


139.5 


107.9 


78.6 


60.9 


61.7 


128.3 


127.7 


112.1 


91.4 


76.8 


77.9 


2.8 


*6.7 


9.1 


8.8 


9.0 


6.4 


*1.3 


*1.4 


0.8 


0.4 


0.5 


0.6 


1.0 


0.8 


0.7 


0.4 


0.3 


4.2 


3.4 


3.0 


1.9 


1.5 


1.7 


15.9 


17.4 


14,3 


8.5 


6.6 


7.0 


75.0 


57.4 


49.1 


31.3 


21.6 


21.6 


248.9 


166.2 


119.4 


81.9 


62.1 


61.9 


567.7 


452.0 


272.5 


187.3 


133.9 


138.7 


754.4 


830.5 


673.4 


502.6 


373.8 


362.2 


496.7 


1,413.1 


1,337.8 


998.2 


865.3 


918.6 


2,578.9 


2,504.8 


2.126.2 


1.881.7 


1,896.3 



Includes deaths of nonresidents of the United States. 
Provisional data. 



^Includes all races and both sexes. 
Age adjusted by the direct method to the total population of the United States as enumerated in 1940, using 11 age groups. 

NOTE: For the data years shown, the code numbers for cerebrovascular diseases are based on the then current International 
Classification of Diseases: for 1950, the Sixth Revision, Nos. 330-334; for 1960. the Seventh Revision, Nos. 330-334; for 
1970-78, the Eighth Revision, Adapted for Use in the United States, Nos. 430-438; and for 1979-82, the Ninth Revision, Nos. 
430-438. 

SOURCES: National Center for Health Statistics: Vital Statistics of the United States , Vol. II, 1950-80. Public Health 
Service. Washington. U.S. Government Printing Office; Annual summary of births, deaths, marriages, and divorces, United 
States, 1982. Monthly Vital Statistics Report . Vol. 31-No. 13. OHHS Pub. No. (PHS) 83-1120. Public Health Service. 
Hyattsville, Md., Sept. 27, 1983; Data computed by the Division of Analysis from data compiled by the Division of Vital 
Statistics; U.S. Bureau of the Census: Population estimates and projections. Current Population Reports . Series P-25, No. 
310. Washington. U.S. Government Printing Office, June 1965; 1950 Nonwhite Population by Race . Special Report P-E, No. 38. 
Washington. U.S. Government Printing Office, 1951; General population characteristics. United States suimiary. 1960 and 
1970. U.S. Census of Population . Final reports PC(1)-1B and PC(1)-B1. Washington. U.S. Government Printing Office, 1961 
and 197?: 



491 



TABLE 3 
Ratio of Stroke Mortality By Age 1980: Black and White 





Black Men/ 
White Men 


Black Women/ 
White Women 


25-34 


3.5 


3.5 


35-44 


4.5 


3.2 


45-54 


3.8 


3.3 


55-64 


3.0 


2.8 


65-74 


2.0 


2.1 


75-84 


1.1 


1.3 


85 + 


0.8 


0.8 


Total 


1.8 


1.8 



Monthly Vital Statistics Reports. National Center for 
Health Statistics, Vol. 33, No. 3, Supplement, June, 1984. 



492 



TABLE 4 



Percentage of Deaths Due to Stroke By Race and Sex 1981 



White Men 
White Women 
Black Men 
Black Women 
Total 



Percent 


5. 


3 


8. 


.1 


7. 


,2 


9, 


.7 


6, 


.7 



Monthly Vital Statistics Reports. National Center for 
Health Statistics, Vol. 33, No. 3, Supplement, June, 1984, 



493 



TABLE 5 







NUMBER OF DEATHS 








1968 - 1970 






Stroke an 

Dnderlyijag 

Cause 


Stroke as 

Associated 

Cause 


Stroke Bot 
Mentioned 


WM 


246,313 


145,496 


2,447,487 


WF 


299,625 


160,170 


1,756,574 


NM 


38,042 


20,653 


348,661 


NF 


41,691 


21,940 


246.305 



625,671 



348,259 



4,799,027 







NUMBER OF DEATHS 








1976 - 1978 






Stroke as 

Underlying 

Canse 


Stroke as 

Associated 

Cause 


Stroke Hot 
Mentioned 


WM 


200,429 


138,515 


2,416,466 


WF 


278,924 


166,131 


1,834,235 


NM 


31,368 


19,216 


351,681 


NF 


35,864 


21.313 


248.673 



546,585 



345,175 



4,851,055 



Personal conrmunication from Herb Baum. 



494 



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■H 


•H 


•H 


to 


to 


CO 


x: 


^ 


iH 


iH 


m 


3 


3 


PQ 


CQ 



(U 



3 



00| 

l-l 
o 

o 





CO 




to 




(U 




Q) 


en 


iH 


to 


i-H 


0) 


to 


tu 


to 


iH 


e 


iH 


s 


to 


tu 


to 


01 


S 


fa 


s 


fa 


(U 


Qi 


^ 


^ 


4-1 


4-1 


u 


CJ 


•H 


•H 


to 


to 


4= 


J= 


iH 


iH 


3 


3 


CQ 


03 



495 



TABLE 7 

Age Specific Stroke Death Rates: 1978 for 
Selected States by Race and Sex/100,000 

Age 45-54 





Georgia 


Pennsylvania 


Colorado 


Mississippi 


All 


White 












Women 


26 


22 


16 


18 


22 


White 












Men 


35 


24 


21 


28 


23 


Black 












Women 


97 


53 


— 


65 


58 


Black 












Men 


143 


92 


— 


116 


81 



Data provided by the National Center for Health Statistics. 



496 



TABLE 8 



Age Adusted Stroke Death Rates By 
Geographic Area 1978/100,000 Ages (35-74) 





White 


White 


Black 


Black 




Men 


Women 


Men 


Women 


Colorado 


43 


38 






Kansas 


50 


43 






Utah 


38 


47 






New York 


48 


39 


91 


75 


Maryland 


47 


38 


115 


73 


South Carolina 


79 


54 


231 


173 


Georgia 


82 


59 


283 


158 


Mississippi 


77 


45 


169 


103 


North Carolina 


70 


47 


197 


145 



Data provided by National Center for Health Statistics. 



497 



TABLE 9 

Age-adjusled death rates per 100,000 (age 40-€9) 

for cerebrovascular disease in Baltimore based 

on inuUiple -cause tabulation of 1960 death 

cerlijlcates by socioeconomic status: 

based on combination distribution of 

socioeconomic areas in whites and 

non-whites* 





Socioecooomic tUtua 


Race & 
sex 


Upper half 


Lower half 






No. 
deaths 


Rate 


No. 
deaths 


Rate 


Unknown 


WM 
WF 

NM 
NF 


85 
73 
26 
43 


129 

90 

280 

410 


78 
77 

108 
124 


189 

174 

422 
472 


1 
2 
2 
2 



*Exclu(iea 30 deathtj in state huHpitub out- 
side Baltimore City. 



Kuller L, Seltser R: Cerebrovascular Disease Mortality in Maryland. 
Am J Epidemiol 1967;86:442-A50. 



498 



TABLE 10 



S60r 



^ Mountain 
"^^ □Pwdmont 
H Ptoins 
^1 Coostal 







vWxte Males While Females Block Moies Siocii F«ro«» 

Age-adjusted mortality rates (per 100.000) for stro^t 
IICU 4 JO to 438) in North Carolina in 1969 according to region o' 
state and sex-race groups (all entries). The numbers within each bit' 
indicate the number of stroke deaths for that region. 



Heyman A, Tyroler HA, et al: Geographic Differences in Mortality 
From Stroke in North Carolina. Stroke 1976;7:41-45. 



499 



TABLE 11 
Stroke Mortality By Age and Sex: Cape Verde Islands (1980) 







Stroke 




U.S. Blacks 




Sex 


Deaths 


Rate/100,000 


1980 


Age 45-54 


M 


10 


128 


82 




F 


12 


131 


62 


55-64 


M 


13 


158 


190 




F 


9 


94 


139 


65-74 


M 


23 


424 


472 




F 


21 


338 


362 



WHO. Statistics Annual 1983. 



500 



TABLE 12 



c 
<u 
u 

0) 

a. 




Percent of Nigerian and Minnesota subjects with cerebral 
atherosclerosis in the presence or absence of hypertension. Note the 
similarity in percent of Nigerian hypertensive subjects and nor- 
molensive Minnesota subjects. 



Williams 0, Loewenson RB, et al: Cerebral Atherosclerosis and Its 
Relationship to Selected Diseases in Nigerians: A Pathological 
Study. Stroke 1975;6: 395-AOl . 



501 



TABLE 13 



Carotid Arteries 



100 

so- 
so- 

70- 
60 
SO 
40 
§ 30 
20 
lO-l 



4j 



^ 



Nftrs-MtlM 






/ • t • • • 



III ^ 4 l^^»,Ji n I 



100 
90 
80 
TO 
60- 
50- 
40- 
»■ 
20- 
lO- 



Whilt-Maln 



*, • • 






20 



— 1 1 " ! 

M 40 



SO 



I ^ I 
60 70 



WkitfFcoMlM 



■ I* !■ I 1 



1 I I * I t I ■• f ^ 



20 30 40 M 60 70 



Age 



Percentage ut iiitiinal surface iavolveii with rui.iuil atheroaclorotic lesions in curotiil arteries 
ui ;iutopsied New Orleans men anti women, basal group oi cases. Each point represents a case; tlie 
trian|$le represents the mean o( the age group. 

Solberg LA, McGarry PA: Cerebral Atherosclerosis in Negroes and 
Caucasians. Atherosclerosis 1972;16:141-145. 



502 



TABLE 14 



Introcronial Arferies 



WO-i 
90 

80 
70 
60 
90 

40- 

I "" 

§ 10- 






I 

I 



lUU- 
90- 


WMtfMalM 


80- 






70- 






SO- 




• 


90- 






30- 

20- 
10- 


■■1 '■■■ »1 


• 

• 



■^*7 • » t 



Mllt-Fa 




20 30 40 50 60 70 

Age 
Percentage of intimal surface involved with raised atherosclerotic lesions in intracranial 
arteries of autopsied New Orleans men and women, basal group of cases. Each point represents a 
case; the triangle represents the mean of the age group. 



Solberg LA, McGarry PA: Cerebral Atherosclerosis in Negroes and 
Caucasians. Atherosclerosis 1972;16:141-145. 



503 



TABLE 15 



Age- and sex-adjusted mortality rates, by ethnicity, Los Angeles County, 1980 







Ane- and 


sex-adjustedf mortality 


rates per 


100.000 population 














Asians and Pacific Islanders 




Log Angeles 


























Cause of death 


County 


While 


Black 


Hispanic} 


Japanese 


Chinese 


Filipino 


Korean 


All causes 


819.9 


870.2 


1038.3 


814.8 


482.5 


362.8 


137.2 


421.8 


Major cardiovascular diseases 


409.4 


429.5 


472.0 


390.6 


255.3 


157.0 


84.2 


143.8 


Diseases of heart 


313.4 


331.2 


353.4 


307.8 


161.7 


99.2 


57.8 


82.1 


Toul IHD 


194.0 


207.7 


192.5 


177.7 


106.9 


47.4 


31.4 


63.9 


MI and other acute IHD 


90.9 


97.9 


88.3 


82.3 


55.4 


28.1 


18.8 


13.1 


Chronic IHD 


103.1 


109.8 


104.3 


95.4 


51.4 


19.3 


12.6 


50.9 


Hypertensive disease 


21.0 


19.5 


47.4 


— 


— 


— 


— 


— 


Gerebrovascular diseases 


74.3 


75.8 


94.2 


63.5 


79.6 


48.7 


19.7 


48.3 



IHC - Ischemic heart disease; MI • myocardial infarction. 

'From Chupman J. Frerichs ft, Maes R: Cardiovascular diseases in Los Angeles, 1980. Los Angeles, 19S3, American Heart Association, Greater Los Angelet 

Affiliate, Inc. 

t Direct method of adjustment with Los Angeles County population, 1980, as standard. 

(Census tracts in which 75 ''i or mure of the population are persons of Spanish-Hispanic origin or descent. 

Haywood LJ: Issues in the natural history and treatment 
of coronary heart disease in black populations: Medical 
management. Am Heart J 1984;108:683-687. 



504 



TABLE 16 



200-1 



■ MALE 

E3 FEMALE 

( ) RATK3 male: FEMALE 




JAPAN 

JAPANESE 

(1.4) 



HAWAII 
JAPANESE 
(1.3) 



HAWAII 


U.S. 


WHITES 


WHITES 


(.94) 


(1.0) 



H970}. 



Age-adjusted stroke mortality 



Kagan A, Popper JS, Rhoads GG: Factors Related to Stroke 
Incidence in Hawaii Japanese Men. The Honolulu Heart 
Study. Stroke 1980;11:14-21. 



505 



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506 



TABLE 18 



3 

a. 
o 
a. 



o 
o 

(T 
UJ 
GL 

> 



o 

z 

a 

}^ 
v> 

D 
-a 
O 
< 
I 
UJ 



4CX)n 



300 



200 



— SSi 




SSO* 

ow? 

0Wo» 



1973 
YEARS 

Secular trends in age-adjusted cerebrovascular 
disease mortality (JCDA codes 430-8) in Bexar County. 
Texas, from 1970-1976 by sex and ethnic group. 

Steru MP, Gaskill SP: Secular Trends in Ischemic Heart Disease and 
Stroke Mortality from 1970 to 1976 in Spanish-surnamed and Other White 
Individuals in Bexar County, Texas. Circulation 1978; 58:537-543. 

SS=Spanish Surname 



507 



TABLE 19 



Average Annual Death Rates from Selected Leading Causes of D<>alti: 

Puerto Rlcan-Born and White Non-Puerto Rican-Born by Age and Sex: 

New Yorl< City, 1969-71 (number of deaths per 100.000 population) 





Males 




Ralio ol naierj o( 

rain-iloe PU»»llO niCan noifl If) 

i-emaies Nor,. Punt io Hiran 
While 


Age 
(yents) 


Puerlo 
nican 


Non-Puerlo 
RIcan While 


Puerlo 
Rican 


Non-Puerlo 
nican While 


Malps f 


■orimlns 




Heart Disease (ICDA- 390-! 


98. 402, 404-2<>) 






25-34 


19 




10 


9 


6 


1 77 


1 49 


35-44 


ns 




94 


30 


27 


90 


1 10 


45-54 


265 




378 


117 


111 


70 


1 rm 


55-64 


616 




995 


393 


347 


or,:? 


1 n 


65-74 


1.610 




2.166 


1,011 


1.10? 


74 


92 


75 and 
over 


2,713 




5,197 


3.037 


4.578 


0.52 


66 


Malignant Neoplasms (ICOA 140-209) 


25-34 


13 




16 


11 


17 


079 


66 


35-44 


48 




52 


53 


75 


0.92 


70 


45-54 


143 




184 


148 


210 


0.78 


70 


55-64 


414 




510 


276 


383 


0.8 1 


7? 


65-74 


726 




1.102 


570 


588 


0.66 


0.97 


75 and 
over 


1.529 




1.768 


886 


1,062 


0.86 


0.03 


Cerebrovascular Disease (ICDA 430-3C) 


25-34 


6 




3 


4 


3 


2.21 


1.10 


35-44 


21 




10 


16 


10 


2.11 


1.G5 


45-54 


44 




29 


36 


25 


1.52 


1.45 


55-64 


97 




80 


92 


59 


1.21 


l.-iH 


65-74 


216 




267 


302 


196 


0.8 1 


1.55 


75 and 
over 


495 




918 


771 


974 


0.54 


0.79 


OlaHntns Mellllus (iCOA ?50) 


25-34 


2 




2 


2 


2 


on? 


".00 


35-44 


7 




6 


4 


4 


1.1? 


O.'in 


45-54 


19 




15 


17 


10 


1.31 


1.73 


55-64 


52 




35 


72 


27 


1.47 


2.60 



Rosenwaike I: Mortality Among the Puerto Rican Born in New York 
City. Social Science (Quarterly 1983;64:375-385. 



508 



Age-specific dsath rates for selected causes, Indian and Alaska Native population in 25 reservation states, 3-year 
average (1973-1975) and U.S. All Races, 1974: rates per 100,000 population 





Under 
1 year 


1-4 
years 


5-14 
years 


15-24 
years 


25-34 
years 


35-44 
years 


45-54 
years 


55-64 
years 


65 Years 
and over 


All Causes 
Indian 


2,342.3 
1,755.7 

127.1 
48.3 

32.2 
7.5 

94.9 
40.9 

49.2 
28.4 

42.4 
22.0 

6.8 
5.1 

0.0 

1.? 
3.8 

239.0 
86.9 

0.5 

1.7 
1.1 

15.3 
2.8 


150.2 
73.9 

80.7 
29.2 

35.8 
9.9 

44.9 
19.3 

5.4 
2.9 

4.6 
2.0 

0.0 

0.8 
0.8 

5.4 
5.9 

-11.7 
4.7 

0.1 

0.4 
0.1 

0.4 
0.4 


63.6 
38.2 

40.4 
18.4 

19.2 
8.7 

21.2 
9.7 

2.9 
1.7 

1.7 
0.9 

0.0 

1.1 
0.6 

0.2 
0.0 

4.0 
5.2 

2.2 

1.3 

0.2 
0.1 

0.2 


376.2 
121.7 

230.5 
61.6 

160.5 
40.5 

70.0 
21.1 

6.9 
4.5 

4.5 
2.8 

0.0 

1.5 
1.4 

0.9 
0.0 

7.1 
6.9 

2.6 
1.7 

0.6 
0.5 

3.4 
0.4 

0.4 
0.4 


578.0 
146.8 

245.1 
45.4 

155.5 
25.3 

89.6 
20.0 

25.4 
14.0 

19.6 
9.4 

0.3 

4.8 
3.6 

1.0 
0.0 

12.7 
15.0 

10.0 
2.5 

3.8 
1.9 

60.8 
4.2 

0.7 
0.4 


773.1 
278.6 

202.0 
40.0 

105.6 
19.0 

96.4 
21.0 

84.4 
72.0 

65.0 
55.7 

1.3 

0.9 

17.2 
13.3 

1.8 
0.2 

37.1 

55.1 

26.5 
5.7 

15.5 
4.3 

139.7 
18.6 

1.8 
1.7 


1,150.7 
675.0 

208.1 
43.5 

97.6 
18.3 

110.4 
25.2 

251.6 
259.8 

192.4 
215.5 

2.8 
2.0 

47.4 
35.3 

7.8 
1.0 

101.5 
183.8 

49.6 
11.1 

35.1 
11.4 

179.0 
38.7 

2.8 
7.0 


1.729.7 
1,549.2 

188.0 
61.2 

85.4 
19.5 

101.7 
31.7 

607.6 
720.9 

451.0 
590.8 

9.2 
4.3 

123.8 
99.6 

23.7 
5.9 

269.0 
437.0 

64.2 
26.6 

86.4 
31.7 

123.8 
50.9 

14.5 
27.3 


4,640.2 


All Races 


6,172.9 


Accidents 

Indian 

All Races 


267.2 
125.0 


Motor Vehicle Accidents 

Indian 

All Races 


90.7 
27.9 


All Other Accidents 
All Races 


174.0 
97.1 


Major Cardiovascular Diseases 
Indian 


2.063.9 


All Races ,- 


3,096.5 


Diseases of the Heart 


1,426.6 


All RAces 


2,758.4 


Hypertension 

Indian 

All Races 


9.8 
25.3 


Cerebrovascular Diseases 

Indian 

All Races 


492.7 
869.0 


Arteriosclerosis 

Indian 

All Races 


83.3 
153.3 


Malignant Neoplasms 

Indian 

All Races 


683.9 
1,040.4 


Influenza and Pneumonia 

Indian 

All Races 


304.0 
200.9 


Diabetes Mellitus 
All Races 


171.6 
132.6 


Cirrhosis of Liver 

Indian 

All Races 


68.6 
42.1 


Bronchitis, Emphysema 
and Asthma 
Indian 


31.9 


All Races 


94.7 



Indian Health Trends and Services. U.S. Department of Health, Education 
and Welfare. Public Health Service, Health Services Administration. 
Publication No. 78-12009. 



509 



TABLE 21 



Age adjusted mortality rates for selected causes among Indians and Alaska Natives in reservation states and the U.S. 

All Races population, 1970 to 1975 







INDIAN AND ALASKA NATIVE 


Cause of death 


Number of 
deaths in; 




Rate per 100,000 Populat 


on 






1975 


1970 


1975 


1974 


1973 


1972 


1971 


1970 


All causes 

Major Cardiovascular Diseases 


5,774 

1,335 

965 

291 

70 

9 

1,256 
704 
552 

508 

355 

281 

145 

64 

27 

185 

180 


5,268 

1,340 

933 

326 

71 

10 

1,116 
595 
521 

421 

276 

314 

143 

63 

33 

125 

105 


824.8 

202.5 

147.4 

43.5 

10.1 

1.6 

170.5 
94.1 
76.4 

79.8 

61.4 

36.1 

23.8 

9.9 

3.7 

26.5 

26.0 


872.6 

235.6 

169.5 

50.1 

12.9 

3.0 

163.2 
86.7 
76.5 

88.4 

66.7 

30.7 

24.4 

9.8 

4.3 

31.7 

21.8 


968.8 

237.0 

167.7 

53.0 

13.4 

2.9 

20Z7 

117.1 

85.6 

81.6 

66.0 

49.9 

28.4 

9.1 

6.9 

31.7 

22.9 


881.6 

229.3 

165.4 

49.0 

6.8 

2.7 

185.1 

107.1 

78.0 

81.3 

60.5 

39.0 

29.3 

10.7 

2.8 

25.7 

20.6 


935.5 

251.1 

182.6 

32.8 

12.0 

2.6 

183.0 
96.5 
86.5 

84.4 

66.8 

41.6 

31.7 

10.6 

6.6 

26.4 

21.8 


889.6 
237.2 


Diseases of the Heart 


168.8 


Cerebrovascular diseases 


55.0 


Arteriosclerosis 


11.8 


Hypertension 


1.7 


Accidents 


181.8 


Motor Vehicle 


98.5 


All Other .- 


83.3 


Malignant Neoplasms 


79.5 


Cirrhosis of the Liver 


56.9 


Influenza and Pneumonia 


46.7 


Diabetes Mellitus 


27.1 


Tuberculosis, all forms 

Bronchitis, Emphysema and Asthma 


11.4 
5.7 


Homicide 


22.2 


Suicide 


17.9 







Indian Health Trends and Services. U.S. Department of Health, Education 
and Welfare. Public Health Service, Health Services Administration. 
Publication No. 78-12009. 



510 



TABLE 22 



K30 
40 


IS 00 


n.0 


\WiQ 


l«M 


M'44 


IH 


X 


i-A 


> ' > 


III! 1 1 




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• 


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" 




\ 


\ 


- 



I<00 ItiO IMP 



9>0 l«40 

I r I' 



1*00 ItiO l»»0 l»M l»40 

I I I I I I ' I , 




l»M tMO 



i>£0 mio 



Course of mortality for selected causes of death in the 
expanding death registration States (logarithmic scale) , 
1900-1945. 

Moriyama IM, Cover M. Statistical studies of heart diseases, 
U.S. Public Health Service, April 23, 1948. 



511 



TABlLE. 23 

AGE ADJUSTED DEATH RATES (ACE 45-74) FOR CEREBROVASCULAR DISEASE 

(UNDERLYING AND CONTRIBUTING) BY RACE AND SEX 

EACH DECADE BALTIMORE AND MEMPHIS* 
IOOOt 

900 
800 

700 
600 



500- 



400- 



O 
o 
o 

» 

o 

~ 3oo-^ 

UJ 



200- 



100 




NM-NF 
NM 




' Bollimore 

— -- Memphis 



Age adjusted to the estimated I960 Baltimore population. 



1930 


1940 


1948 


I960 


31 


41 


49 


61 



Kuller L, Seltser R, Paffenbarger RS , Krueger DE. Trends in 
cerebrovascular disease mortality based on multiple cause 
tabulation of death certificates 1930-1960. Am J Epidemiol 
1969;88:307-317. 



512 



TABLE 24 



Age Adjusted Annual Decrease in Stroke Mortality 
1968-1978 By Race and Sex in Percentage 



White White Black Black 
Women Men Women Men 



1968-1978 


5.0 


4.6 


5.5 


6.8 


1968-1973 


2.0 


2.3 


3.1 


3.6 


1974=1978 


7.8 


6.8 


6.7 


8.8 



Arteriosclerosis 1981, Vol. 2. U.S. Department 
'of Health and Human Services, PHS NIH # 82-2035. 



513 



Table 25 

Trends of Mortality Rates from Cerebrovascular Diseases (ICD 430-438), 

Age-Adjusted, Persons Age 35 to 74 by Sex-Color, 

United States, 1968-78 







White 


White 


Nonwhite 


Nonwhite 




Year 




Men 


Women 


Men 


Women 


All 


1968 




155.4 


110.8 


340.2 


292.1 


148.1 


1969 




150.3 


106.8 


317.1 


274.3 


142.2 


1970 




146.8 


105.8 


304.0 


261.9 


139.3 


1971 




143.8 


100.7 


292.9 


248.6 


134.2 


1972 




144.8 


99.7 


280.4 


249 .8 


133.6 


1973 




137.4 


96.8 


282.0 


239.8 


128.7 


1974 




129.4 


91.3 


260.8 


216.6 


120.7 


1975 




117.8 


83.7 


233.7 


190.1 


109.7 


1976 




108.9 


78.5 


216.6 


176.9 


102.2 


1977 




100.9 


72.4 


202.2 


162.4 


94.6 


1978 




93.9 


68.7 


194.7 


148.6 


88.7 


Change 1968 


1-78 


-62.1 


-42.1 


-145.5 


-143.5 


-59.4 


Percent Change 


-40.0 


-38.0 


-42.8 


-49.1 


-40.1 


Slope 1968- 


•73 


-0.0174 


-0.0190 


-0.0348 


-0.0359 


-0.0288 


Standard Error 


0.0035 


0.0036 


0.0049 


0.0048 


0.0032 


Slope 1973- 


■78 


-0.0789 


-0.0707 


-0.0769 


-0.0951 


-0.0761 


Standard Error 


0.0017 


0.0021 


0.0054 


0.0041 


0.0020 



Report of the Working Group on Arteriosclerosis of the National 
Heart, Lung and Blood Institute. Arteriosclerosis 1981. 
Volume 2. 



514 



TABLE 26 



Average 
annual 

incidence 
rates 



300 



200 



70 
60 

so 



10 



Men 



Women ^^ ^^"^ 



1945-49 19&S-59 1965-69 1975-79 
1950-54 1960-64 1970-74 

Calendar years 

Fi\i'-Year averoiie annual incidence rates per 
lUUMOO populalion for all first episodes of stroke in men and 
women in Rochester, Minneuua, age adjusted to I960 PS white 
population. 

Whisnant JP: The Decline of Stroke. Stroke 1984;15:160-168. 



515 






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516 



TABLE 28 



Trends in Stroke Mortality 1974-1978 By State: In 
Percent, Annual Change, Age Adjusted (35-74) 





White 


White 


Black 


Black 




Women 


Men 


Women 


Men 


Colorado 


6.6 


6.7 






Connecticut 


9.2 


6.0 






Massachusetts 


10.0 


11.0 


18.2 


-1.0 


Maryland 


6.9 


8.2 


11.2 


6.1 


North Carolina 


4.8 


9.1 


10.9 


7.3 


Pennsylvania 


6.8 


8.4 


9.0 


8.3 


Georgia 


6.7 


6.1 


10.4 


6.1 


South Carolina 


5.8 


10.9 


6.4 


6.6 


Mississippi 


5.0 


10.0 


9.9 


5.3 



National Center for Health Statistics. 



517 



ao 












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ro 


m 


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00 






CM 

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o 
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to ^ 

0) 
■l-l u 

(£! a. 

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n) 00 

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Q) xt 

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c 

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en 
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60 





fO 


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a 


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m 


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CM 


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CM 


1—* 


















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u 























o <r O o r-. -* 

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ON CN ^ >-( ^ 






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518 



TABLE 30 



Percentage Decline in Stroke Mortality 
By Age, Race and Sex 1970-1980 





WM 


WW 


BM 


BW 


1 

35-44 


44.9 


41.7 


44.6 


56.0 


45-54 


39.0 


38.7 


39.8 


48.2 


55-64 


47.6 


37.6 


44.8 


48.9. 


65-74 


42.9 


43.0 


39.3 


46.2 


75-84 


37.2 


37.9 


26.0 


31.3 



Health United States, 1983, 



519 



TABLE 31 



500- 



400- 



i 300> 



I 250 



200 



S 






150 



100 

9C 
80 



TAIWAN 





J I « ' ■ t I ' ' ' I I I I I L 



J I L 



1955 



1960 



1965 



1970 



1975 



Mortality from cerebrovascular disease in population aged 55-64, (1 955-1 974). 

Tseng WP, Epidemological study of hypertension and stroke in 
Taiwan. In: Prophylatic Approach to Hypertensive Diseases , 
Y. Yamori et al. (eds.), Raven Press, New York, 1979. 

520 



TABLE 32 



Age-Specific Prevalence Rates of Stroke (per 1,000) Found in Examination, 1967 Through 1969 



Age 
At Time of 
First Exam- 
ination, yr 



White Men 



White Women 



Black Men 



Black Women 



Population 
Examined 



No. of 
Cases 



Rate 



Population 
Examined 



No. of 
Cases 



Rate 



Population 
Examined 



No. of 
Cases 



Rate 



Population 
Examined 



No. of 
Cases 



Rate 



S34 


193 






•> 196 


1 


5.1 


82 






110 






35-44 


152 


3 


19.7 


175 






63 


2 


31.7 


93 


2 


21.5 


45-54 


223 


9 


40.4 


221 


2 


9.0 


133 


9 


67.6 


147 


7 


47.6 


55-64 


138 


7 


50.7 


161 


5 


31.0 


61 


5 


82.0 


109 


2 


18.3 


S65" 


60 


9 


150.0 


102 


3 


29.4 


47 


2 


42.6 


59 


7 


118.6 


Total 
S35yr 


573 


28 




659 


10 




304 


IS 




408 


18 




All ages 


771 


28 




855 


11 




386 


13 




518 


IS 




Age-adjusted rate 
S35 






53.2 






15.0 






58.6 






43.4 


All ages 






40.9 






12.7 






45.0 






33.4 



* Only 11 persons were greater than 75 years of age, two of whom had cerebrovascular disease. 

Heyman A, Karp HR, Heyden S, et al: Cerebrovascular Disease in the 

Biracial Population of Evans County, Georgia. Arch Intern Med 1971;128:949-955. 



521 



TABLE 33 



Pravalenca o/ stroke In examined cohorts aa determined tjy neurologists 







Japan" 




Hawaii* 


California' 


















Significance 












^^^" 




Age group 


N 


Rata/ 1.000 


N 


Rate/ 1.000 


N 


Rate/ 1.000 


level^ 








Definite cases only 








45-49 





— 





— 


2 


2.7 


NS 


50-54 


5 


20.3 


14 


4.9 


4 


7.6 


<0.02 


55-59 


16 


41.3 


12 


6.2 


2 


7.4 


<0.001 


60-64 


19 


49.5 


25 


19.2 


3 


18.1 


<0.01 


65-69 


28 


72.4 


29 


34.2 


3 


19.4 


<0.01 


Total 


68 


46.6 


80 


10.7 


14 


7.6 




Ao*-ad|ustad 




35.4 




10.7 




10.4 




rate' 




Definite and possible cases 






45-49 





— 


1 


2.0 


4 


5.5 


NS 


50-54 


7 


28.5 


21 


7.3 


5 


9.6 


<0.01 


55-59 


17 


43.9 


18 


9.3 


3 


11.0 


< 0.001 


60-64 


23 


59.9 


31 


23.8 


3 


18.1 


<0.01 


65*69 


33 


85.3 


41 


48.4 


4 


25.8 


<0.01 


Total 


80 


54.9 


112 


15.0 


19 


10.3 




Age-adjusted 




42.5 




15.0 




13.0 




rate' 

















"In Japan,- 85% of definite and possible stroke cases were seen by tlie neurologist. 
Remaining cases diagnosed by neurologist from review of clinic records and occasionally 
Irom hospital records. 

" In Hawaii. 62% of definite and possible stroke cases were seen by tne neurologist. 
Remaining cases diagnosed by neurologist from review of clinic and hospitalization 
records. The latter were usually available. 

'' In California, 74% of definite and possible stroke cases were seen by the neurologist. 
Remaining cases were classified as definite stroke or no stroke on the basis of the screen- 
ing test results. 

'' Chi square test with two degrees of freedom. 

' Age-adjusted by direct method to age structure of Hawaii cohort. 



Kagan A, Popper J, Rhoads GG, et al: Epidemiologic studies 
of coronary heart disease and stroke in Japanese men living 
in Japan, Hawaii, and California: Prevalence of stroke. 
CerebrjQvascular Diseases , edited by P. Scheinberg, Raven 
Press,- New York, 1976. 



522 



TABLE 34 



Number of Hospital Discharges* for Stroke 
By Race and Average Length of Stay 1981 



Discharges 
(in 1. OOP's) 



Average Length of Stay 
(Days) 



White 707 

All Others 100 

Total 806 

*First Level Diagnosis Only 



12.2 
14.2 
12.4 



National Center for Health Statistics, Hospital Discharge Survey. 



523 



TABLE 35 



Stroke Economic Costs (1980) 



>5% 



Total $5.1 Billion 

Hospital 52% 

Nursing Home 35% 

Professional Ser. 11% 

Drugs 2% 

Per Capita 

<65 Men $8 
Women $ 7 

>65 Men $128 
Women $147 

Total 



Per Capita <65 Men $627 
Women $791 

>65 Men $2,278 
Women $2,667 

Health Care Financing, Summer, 1984. 



524 



TABLE 36 



Sitinlur (1/ ('rMo uiut huijfiui'' KiiU\ tor Slinkv. Smilli .\Uihiiiiui Sliiih I'l'i'iiliilimi. IVfUl 



While 




lain 


M.1I0 
ilvr <»1' xir4»ke% 




Female 
number oi' sirnko 


t 


Tiilal 
lumber nl' sirokes 


A^e 


All 


l-ilvl 


Incidence 
rales 


All 


Hirvi 


Incideiwe 
rules 


All 


Kirsi 


lneiderH.e 
rules 


:m-.m 


5 


4 


4V 


4 


3 


35 


9 


7 


42 


55-64 


5 


5 


274 


6 


5 


233 


II 


10 


252 


65-74 


X 


7 


541 


6 


6 


365 


14 


13 


442 


75 + 


II 


li» 


1.3X5 


K 


S 


719 


19 


IX 


9X1 


All asjes 


2V 


26 




24 


n 




53 


48 




Cnidc rate 






136 






107 






121 


Apc-adjusied 


raic+ 




139 






88 






109 


Black 




Ntaie 

number tif sjntkcb 




Female 
number of sirokes 


TomJ 
nunibcr' uf strokes 


Age 


All 


Firsl 


Incidence 
rales 


All 


Firsi 


Incidence 
rales 


All 


Hrst 


Incidence 
rales 


2U-54 


7 


3 


32 


9 


X 


64 


16 


11 


50 


55-64 


14 


13 


566 


19 


18 


712 


33 


31 


642 


65-74 


16 


14 


1.IU6 


m 


16 


957 


35 


30 


1.021 


75 + 


5t 


3 


482 


IX 


16 


1.824 


23 


19 


1.268 


All aces 


42 


33 




65 


58 




107 


91 




Cnidc ra(c 






MO 






174 






144 


Age-adjuMcd 


raiet 




172 






236 






208 



*Ralc of initial sirokes per KW.OOO persons. 

'i'Aiic-adjusicd rales based on the .MSCDS National Survey uf Stroke." indirect method. 

lOnc case had unknou n |xior stroke history in each of these categories. 

Gross CR, Kase CS, et al: Stroke in South Alabama: Incidence 
and Diagnostic Features— A Population Based Study. Stroke 1984- 
15:249-255. ' 



525 



TABLE 37 



F<«*-y««r incldanca a( lalal and nonfatal atroka by raoa and ••* ioi Siappad Car* 
(SO and Ralarrad Cara (RC) participanla. Data ara adiualad lor aga and antry diaaloUc 
blood praaaura. Shadad portion indicalaa latat atrofca; «»hita portion, nontalal alroka. 



2.9 



m 

RC 



i 



1 a 



•^sc 



34 64 



37 



RC 



{ ie.2% r— - 

J 33 



3.1 



m 




46.6% 



2.6 



m 



i 



t.ft 



^ 
^ 



40.0% 



2.3 



7^' 




auck Mmi 



Black WontMi 



W»ul« Man 



Wluia Woman 



Five-Year Findings of the Hypertension Detection and Follow-up 
Program. Ill, Reduction in Stroke Incidence Among Persons 
with High Blood Pressure. JAMA 1982;247:633-638. 



526 



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527 



TABLE 39 



Avciiif-f Atimiiil ImiJiiu <- <// Dttinilc uiul PnwihU- Slmki- /H'r IIMXI by Afif 







Japan IV72-7K 






Hawaii 1965-73 








No. <i| 


N<i. of 




No. of 


No. of 






Ai:c 


^iihjivls 


tav-'s 


Raiot 


Mibjccls 


cases 


Kate 


Ti-sttt 


45-4V 


54 





0.0 


1K25 


II 


1.0 


NS 


50-54 


2.W 


7 


7.3 


2766 


39 


2.3 


*« 


55-59 


.V.7 


II 


7.5 


1569 


21 


2.2 


•♦*• 


60-64 


357 


17 


11.9 


1306 


37 


4.7 


»*• 


65-6V 


549 


27 


19.3 


429 


18 


7.0 


*»• 


Toul 


I.V>6 


f>l 


11.3 


7895 


126 


2.7 




Age adjuMod raic+tt 






7.4 






2.7 


*»• 



tAnnuai IncitJonce rate is calculated as follows: Japan: (No. of cases/No. of subjccls)'4 (Years follow-up). Hawaii: 
(No. of cases/No. of subjecls|.6 O'ears follow-up* 

■f-fy.- lesi of two rales between two cohorts NS: /> > 0.10. ': p < 0.05. '♦: p OO.OI. *■'*■. p < 0.00! 
t'i'tCalculated by (he indirect method with Hawaii as siandiird 

Takeya Y, Popper JS, et al: Epidemiologic Studies of Coronary 
Heart Disease and Stroke in Japanese Men Living in Japan, Hawaii 
and California: Incidence of Stroke in Japan and Hawaii. 
Stroke 1984;15:15-23. 



528 



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529 



TABLE 41 



Overall huideme Rales' for Strukt by Diaiciutuic CaU'cory, Rate ami Sex South Alabama Study Population, 19fW 







Toial* 






Diagnosis 








Athero- 
thrombotic 
infarction 


Unspecified 

origin 
infarction 


Embolic 
infarction 


Lacunar 
infarction 


Parenchy- 
matous 
hemorrhage 


Subarachnoid 
hennirrhagc 


All case« 




I60(IOO»t 


9(6) 


64(40) 


42(26) 


20(13) 


43(8) 


9(6) 


crude rale 




282.4 


15.9 


113.0 


74.1 


3SJ 


22.9 


15.9 


While 


















male 


number 


29( 100) 





9(31) 


12(41) 


5(17) 


2(7) 







rate 


242.7 





75.3 


100.4 


41.8 


16.7 





female 


number 


24(l()0) 





10(42) 


6(25) 


2(8) 


1(4) 


3(13) 




rate 


177.3 





73.9 


44.3 


14.8 


7.4 


22.2 


Black 


















male 


number 


42(100) 


5(12) 


1.^(31) 


15(36) 


4(10) 


5(12) 







rate 


307.5 


36.6 


95.2 


109.8 


29.3 


36.6 





female 


number 


65( 100) 


4(6) 


32(49) 


9(14) 


9(14) 


5(8) 


6(9) 




rate 


371.2 


22.8 


182.8 


51.4 


51.4 


28.6 


.^.3 



*A1I strokes per lOO.OtXI persons aped 20 and over. 

^Includes 1.^9 initial stroke case*. 19 recurrent stroke cases. 2 cases with unknown CVD history. Three cases which had other stroke 
diagnoses arc in the total hut not listed by diagnosis. 

^Numbers in parentheses arc the piuf>i<nions of cases in each diagnostic catcgoiy. 



Gross CR, Kase CS, et al: Stroke in South Alabama: 
and Diagnostic Features — ^A Population Based Study. 
15:249-255. 



Incidence 
Stroke 1984; 



530 



TABLE 42 



.\'imihi-r III Siroki- C"<i.v<'v In Si(lil\pe iiiitl Cirlainiy 
Ditiviiini.s — Jujum iiiul Hawaii 







Jupun 






Muwuii 








Dcli- 


Pos- 




Dcii- 


l>l)S- 


Subiypc 


Toial 


nitc 


sible 


T»)lal 


ni(c 


sihlc 


Toial 


•62 


38 


24 


126 


71 


55 


ICH 


IK 


12 


6 


34 


26 


H 


T-E 


44 


26 


18 


74 


42 


32 


Unknown 











IK 


3 


15 



Takeya Y, Popper JS, et al: Epidemiologic Studies of Coronary 
Heart Disease and Stroke in Japanese Men Living in Japan, Hawaii 
and California: Incidence of Stroke in Japan and Hawaii. 
Stroke 1984;15:15-23. 



531 



TABLE 43 



Average Annual Stroke InciJcnce Per 1000 h\ Agtf uml Subtype — Definite Cases Only 









Total 




Inlrjcranial 


hcnKirrhagc 




Throiiilxicmbolic stroke 




Jai 


pan 


Haw 


aii 


Japan 


Haw 


aii 


Japan 


Hawaii 


Age 


No. of 
cases 


Rate 


No. .if 

cases 


Rate 


No. of 

cases 


Rate 


No. of 

cases 


Rale 


No. of 

cases 


Rate 


No. i>l 

cases Rale 


4.^-49 





0.0 


6 


0.55 





0.0 


2 


0.18 





0.0 


3 i).;7 


50-54 


6 


6.3 


22 


1.3 


4 


4.2 


10 


0.60 


1 


2.1 


II 0.66 


55-59 


7 


4.8 


13 


1.4 


2 


1.4 


3 


0.32 


5 


3.4 


10 I.I 


(n-M 


II 


7.7 


tt 


2.7 


1 


1.4 


9 


I.I 


9 


6.3 


12 1.5 


65-69 


14 


10.0 


9 


3.5 


4 


2.9 


•> 


0.77 


10 


7.2 


6 2.3 


Tiiial 


.^U 


7.0 


71 


1.5 


12 


2.2 


26 


0.55 


26 


4.S 


42 II. S9 


Age ad- 
justed 

rule 




4.7 




1.5 




1.7 




0.55 




3.0 


SV 



Takeya Y, Popper JS, et al: Epidemiologic Studies of Coronary 
Heart Disease and Stroke in Japanese Men Living in Japan, Hawaii 
and California: Incidence of Stroke in Japan and Hawaii. 
Stroke 1984;15:15-23. 



532 











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533 



TABLE 45 



Prevalence rates of elevated blood pressure levels* for black persons 

25-74 years by sex and age: United States, 1971-75 and 

1976-80. 



Sex and Age 



Elevated blood pressure* 



1971-75 

Standard 



1976-80 



Rate 



error 



Rate 



Standar"? 
error 



Men 

Age-adjusted+ rate for 25-74 years. 

25-34 years 

45-44 years 

45-54 years 

55-64 years 

65-74 years 

Wonen 

Age-ad justed+ rate for 25-74 years. 

25-34 years 

35-44 years 

45-54 years 

55-64 years 

65-74 years 



35.7 



30.5 



Per 100 population 



3.7 23.1 1.8 



16.4 


5.7 


11.7 


2.4 


37.7 


8.8 


22.3 


4.4 


34.7 


6.8 


23.0 


5.7 


59.9 


6.5 


39.2 


4.5 


43.7 


8.0 


27.5 


3.0 



2.7 



24.4 



2.4 



12.4 


5.1 


4.3 


1.5 


23.9 


5.7 


17.6 


4.1 


39.4 


5.4 


37.5 


5.6 


46.0 


7.4 


36.4 


6.2 


46.7 


6.7 


43.4 


5.8 



i 



* Systolic blood pressure of at least 160 mm Hg and/or diastolic blood pressure of 
at least 95 mm Hg. 

+ Age adjusted by direct method to the total U.S. population as estimated at the 
midpoint of the 1976-80 National Health and Nutrition Examination Survey. 

SOURCE: Division of Health Examination Statistics, National Center for Health 

Statistics: Data from the National Health and Nutrition Examination Survey. 



Rowland ML, Fulwood R: Coronary Heart Disease Risk Factor 
Trends in Blacks Between the First and Second National 
Health and Nutrition Examination Surveys, United States, 1971-80, 
Presented at American Heart Association Symposium on Coronary 
Heart Disease in Black Populations, March 5, 1983. 



534 



TABLE 46 



Mean systolic blood pressure ( ^SD) in Laredo Project participants and HANES I subjects, by sex 





n 


Laredo 
Project 




HANES Id) 




Age 
(years) 


"Spanish- 
Mexican 
American" 


US 
white 


US 
black 








Men 






35-44 


18* 


129.2 = 19.1 


124.7 * 12.8 


127.0 r 14.8 


136.7 - 18.8 


45-54 


37 


134.4 * 18.1 


140.1 * 15.0 


134.7 * 19.7 


141.7 * 28.2 


55-64 


42 


132.1 r 25.7 


139.9 rr 19.9 


139.6 r 20.4 


144.2 i 23.0 


65-74 


30 


150.3 i 29.2 


146.0 r 19.4 
Women 


146.0 = 24.1 


156.6 - 28.3 


35-44 


34* 


119.2 - 20.6 


122.4 = 19.8 


122.6 * 18.7 


130.5 = 21.4 


45-54 


93 


126.9 * 18.3 


130.0 r 17.5 


131.1 ± 22.2 


150.8 r 35.1 


55-64 


70- 


134.8 = 21.6 


144.8 T 28.0 


143.0 = 25.2 


153.4 - 27.4 


65-74 


65 


155.7 * 25.5 


150.1 = 21.2 


151.6 r 24.7 


161.3 r 28.7 



Mean diastolic blood pressure ( ^SDj in Laredo Project participants and 

HANES I subjects, by sex 









Men 






35-44 


18- 


89.6 - 13.3 


81.8 ± 9.7 


84.2 * 11.3 


91.2 ± 12.1 


45-54 


37 


88.3 £ 10.6' 


86.5 ± 9.3 


87.5 ± 12.7 


91.9 * 16.5 


55-64 


42 


82.6 * 12.6 


86.8 ± 7.3 


86.4 * 12.0 


93.4 r L4.1 


65-74 


30 


84.5 ± 11.5 


82.4 * 10.6 
Women 


84.9 i: 13.0 


90.9 = 14.0 


35-44 


34* 


79.2 * 13.0 


78.3 i 11.8 


79.3 ± 12.0 


86.9 i 13.7 


45-54 


93 


80.5 £ 9.3 


83.7 - 10.5 


82.6 ± 13.1 


93.5 ± 15.3 


55-64 


70 


80.9 ± 10.3 


85.8 ± 9.9 


86.2 * 12.4 


90.6 2 13.9 


65-74 


65 


77.5 i 12.4 


81.6 - 10.8 


85.4 * 12.5 


90.4 = 15.9 



Age range 40-44 years for Laredo Project participants. 

Stern MP, Gaskill SP, Allen CR, et al: Cardiovascular Risk Factors in 
Mexican Americans in Laredo, Texas. Am J Epidemiol 1981;113:556-562. 



535 



TABLE 47 



Systolic blood pressure levels by age and sex amoag Minneapolis American Indians and Twin Cities whites 

























Clinical screenings 


(iL-hites) 






Little Earth 






Other 


site screenings 










Average 










Aunrage 


second/ 








Average second! 








second/ 






First SBP 


third SBP 




First SBP ' 


third SBP 




First SBP 


third SBP 




n 


X 


(SD) 


X 


(SD) 


n 


X 


(SD) 


X 


(SD) 


n 


X 


(SD) 


X 


(SD) 


Men 
15-24 


13 


119.5 


(15.3) 


117.5 


(14.3) 


36 


121.7 


(11.6) 


120.6 


(13.1) 












25-34 


U 


121.5 


(13.3) 


120.4 


(13.3) 


49 


125.2 


(13.8) 


125.3 


(13.2) 


265 


117.7 


(11.5) 


117.7 


(11.1) 


35-54 


13 


138.2 


(17.8) 


139.4 


(18.9) 


32 


127.1 


(U.7) 


126.8 


(U.7) 


419 


121.4 


(13.9) 


121.4 


(13.5) 


55-34 


8 


136.8 


(19.0) 


131.5 


(15.8) 


10 


138.0 


(19.1) 


141.2 


(17.3) 


235t 


131.1 


(17.6) 


131.0 


(17.1) 


All ages 


45" 


128.5 


(18.1) 


127.2 


(17.9) 


127* 


125.7 


(13.7) 


125.6 


(14.0) 


919 


122.8 


(15.3) 


122.8 


(14.9) 


Women 
































15-24 


34 


114.3 


(10.3) 


113.2 


(10.2) 


35 


113.7 


(12.6) 


112.8 


(12.2) 


— 










25-34 


33 


112.9 


(10.6) 


113.8 


(11.0) 


42 


115.4 


( 9.2) 


117.0 


(13.0) 


343 


108.5 


(11.3) 


103.5 


(ll.O) 


35-54 


25 


122.D 


(17.1) 


123.4 


(18.6) 


40 


122.9 


(12.0) 


122.9 


(13.7) 


451 


116.1 


(14.9) 


116.0 


(14.8) 


55-34 


13 


129.1 


(10.1) 


129.7 


( 8.2) 


15 


132.1 


(21.2) 


133.3 


(18.9) 


237t 


134.3 


(19.5) 


133.5 


(19.0) 


AH a,;es 


105* 


117.7 


(13.6) 


U7.8 


(13.9) 


138* 


119.3 


(13.8) 


119.6 


(15.0) 


1031 


117.8 


(13.4) 


117.6 


(18.0) 



SBP = ivstolii: blood pres:iure 



'SxrluJes pa/ticipanLs with miasinif age. sex, or blood pressure data. 

*^win Citie:, whites, 55 to 7-4 years old. 

Gillum RF, Gillum BS, et al: Cardiovascular risk factors among urban 
American Indians: Blood pressure, serum lipids, smoking, diabetes, health 
knowledge, and behavior. Am Heart J 1984;107:765-777. 



536 



TABLE 48 



Systolic Blood Pressure Medians by 
Age, Area, and Generation 
nimHg 

150 





IIV 


■--.:.\::-:v TV- 


t^^mt « ifm^^ 






• ■ ■ _ : - '- • • 


^^^^ / 






■::;■■' ^■:'--- As 


/--' 


z 

< 




CALIF NISEI .•'^ .• 


/^•^ 






f-'^' 


a 


130 






f* 




HAWAII - / , 


-. 


» 




NISEI ./>? 




en 




HAAVAII/y?* 
ISSEI .•'/.• 






120 


JAPAN ^i 

• 

•' CALIF ISSEI 





■15-49 50-54 55-59 60-64 C5-<>9 

AGE 



Winkelstein W, Kagan A, Kato H, Sacks S: Epidemiological 
Studies of Coronary Heart Disease and Stroke in Japanese 
Men Living in Japan, Hawaii and California: Blood Pressure 
Distributions. Presented at 101st Annual Meeting, 
American Public Health Association, San Francisco, California, 
November, 1973. 



537 



TABLE 48 (cont.) 



Diastolic Blood Pressure Medians by 
Age J Area, and Generation 
mm Hg 

100 ,,- ., ••.-■• :.■■- 



90 



CU.IF NISEI 



z 

< 



^ 80 



CALIF ISSErX 



Q 




70 



45-49 50-54 55-59 60-64 63-69 
AGE 



Winkelstein W, Kagan A, Kato H, Sacks S: Epidemiological 
Studies of Coronary Heart Disease and Stroke in Japanese 
Men Living in Japan, Hawaii and California: Blood Pressure 
Distributions. Presented at 101st Annual Meeting, 
American Public Health Association, San Francisco, California, 
November, 1973. 



538 



TABLE 49 



Systolic Blood Pressure Msdians* Adjusted to Relative 
Weight Differences by Age, Area and Generation: 
Japan, Hawaii and California 
(Unadjusted medians shown in parentheses) 



Age 



45 - 49 



50 - 54 



55 - 59 



GO - 64 



65 - 69 



Japan 


Hawaii 


Califoi 


nia 




Issei 


Nisei 


Issei 


Nisei 


123 


124»* 


122 


119** 


129 


(120) 

j 


(122) 


(128) 


(118) 


(130) 


127 


125 


124 


127 


132 


: (128) 


(128) 


(130) 


(128) 


(136) 


131 


130 


126 


132 


141 


; (130) 


(132) 


(132) 


(140) 


(140) 


138 


130 


132 


140 


134 


■ (138) 


(134) 


(136) 


(144) 


(140) 


142 


134 


136 


146 


135 


(140) 


(140) 


(138) 


(146) 


(142) 



• Median = iiicuii oE medians fiom the relative weight groups: 
< 00, 00-100, 100-110, 110-120, 150-130. > 130. 

•• Values bused on n < 30. 

Winkelstein W, Kagan A, Kato H, Sacks S: Epidemiological 
Studies of Coronary Heart Disease and Stroke in Japanese 
Men Living in Japan, Hawaii and California: Blood Pressure 
Distributions. Presented at 101st Annual Meeting, 
American Public Health Association, San Francisco, California, 
November, 1973. 



539 



TABLE 50 



MEN 



180 



en 



uo 






o 
o 

ffl 



100 



60L- 



US. 1960-62 

— — Framinghom. Moss. 
— — Taipei. Toiwon 



Japanese 
Nutriticx\ 
Taivyan, 1976 



SYSTOLIC 




DIASTOLIC 




£ 



20 30 ^0 50 

Age (in years) 



60 



76 



60 



M&an blood pressure, by. age for men: five surveys. 



Tseng WP. Epidemiological study of hypertension and 

stroke in Taiwan. In: Prophylactic Approach to Hypertensive 

Diseases , Y. Yamori et al. (eds.), Raven Press, New York, 1979, 

540 



TABLE 51 



Prevalence of Hypertension for Japanese Males 
by Age and Geographical Location 



Age 


Japan Hawaii California 
Deflnite Hypertension 
(Prevalence! 1000) 


Japan Hawaii California 
Borderline Hypertension 
(Prevalence/ 1000) 


45-49 


139 


142 


234 


163 


222 


306 


50-54 


194 


183 


286 


203 


221 


280 


55-59 


255 


199 


263 


199 


252 


253 


60-64 


280 


247 


384 


239 


236 


292 


65-69 


318 


352 


423 


278 


288 


245 


Age-Adjusted Rate 


223 


194 


315 


215 


235 


285 


No. of men 


2127 


7998 


1795 


2127 


7998 


1795 



Winkelstein W: Cooperative studies of blood pressure in 
Japanese in Japan, Hawaii and the United States. In: 
Epidemiology and Control of Hypertension , edited by 
Oglesby Paul, Stratton Intercontinental Medical Book 
Corporation, 1975. 



541 



TABLE 52 



fravalence of lert-vemricutar hyiwuwipfcy mad hyi 
MM iM» bjrgcofraphicil lontici*. 


rananaiwa haan i 


ttaaaaa amaiig Jap» 




Ap-Mliuiud pwvilinci/IOOO 




»«^ 


Japan 
to -2137) 


Hawaii 
to • 799«) 


CalUbma 
to -IT*)) 


LtA-vamricutar hypanrephy * 
HypHwmiv* haan dimM^ 


My4 


J.; 
u 





* UA-vamncuiar hypcruophy « Minoama Codas 3-4 

* EM nita hypanamion (syitaiic > MA 
'-flypan#qp»]r. 



fta»4-l, 4-3 or 4-3 Pius S-i. S-2 or 



>«S 



542 



TABLE 53 



Number of subjects and mean values of selected characteristics, by company and amplitude of R^waves. 



Selected characteristics 





NTT 






AT&T 




High 


R-wave* 


Normal 


High 


R-wave* 


Normal 


3-1 


3-3 


R-wave 


3-1 


3-3 


R-wave 


120 


68 


638 


43 


17 


899 


48.4 


48.6 


47.9 


43.6 


44.6 


45.2 


4.1 


4.1 


4.0 


5.0 


4.7 


5.5 


8.7 


8.6 


8.4 


12.3 


n'.s 


12.5 


16.7 


17.2 


16.5 


17.5 


16.5 


19.8 


15.1 


16.3 


14.3 


24.8 


27.2 


27.4 


131.2 


133.3 


123.4 


123.1 


130.8 


120.2 


88.3 


87.5 


83.2 


88.0 


90.0 


86.4 


84.6 


83.9 


79.8 


78.9 


79.8 


76.6 


13.1 


12.7 


12.7 


14.0 


13.4 


13.8 


28.3 


28.4 


28.3 


31.7 


32.1 


32.7 


0.463 


0.447 


0.449 


0.442 


0.417 


0.422 


68.4 


68.1 


70.2 


70.2 


68.1 


70.5 


88.9 


90.7 


91.4 


92.5 


90.7 


90.6 


20.5 


22.6 


21.2 


22.3 


22.6 


20.1 


196.2 


201.1 


201.8 


232.0 


233.2 


234.2 


134.5 


162.4 


141.2 


125.4 


100.9 


137.6 



Number of subjects 
Age, years 
Skinfolds, mm. 

Ulnar 

Triceps 

Subscapular 

Abdominal 
Blood pressure, mm Hg 

Systolic 

Diastolic 1 

Diastolic 2 
Heart and Chest Size 

Heart diameter, cm 

Chest diameter, cm 

Cardio-thoracic ratio 
Pulse, beats/minute 

Resting 

After exercise 

Increase 
Serum lipids, mg% 

Cholesterol 

Triglycerides 



• See text for definitions. 



Sasaki S, Coiustock GW, et al: High Amplitude R-Waves in Japanese 
and American Telephone Executives. International Journal of 
Epidemiology 1978;7:73-77. 



543 



TABLE 54 

Prevalence of EGG Abnonnalities at Baeeline for MFFIT Men 

With Screen 1 DBP >95 :nii Hg and Screen 2 DBP >_90- inm Hg by Color 



Abnormality 

Q~QS 

ST Depression (4.1-4.3) 

Negative T Waves (5.1-5.3) 

A-V Conduction Defects (6.1-6.S) 

Ventricular Conduction Defects 
(7.1-7.8) 

Lhythn (8,1-8.6) 

Low QRS (9.1) 

ST Elevation (9.2) 

Lei'c Aiiin deviation (_<30'') 

Rlpht Axis deviation (>4-120°) 

IJlgh R - left (3.1) 

High R - right (3.2) 

High R (3.3) 

5. 1-5. 3 1 or left axis deviation 
_<-20°, or 3.1 or 3.3 

Any AbnorEality 







Non- 


black 






Black 


(n=523) 


(N 


=6367) 


Total 
No. 


(N=6995) 


Kg. 


Percent 


No. 


Percent 


Percent 


18 


2.9 


95 


1.5 


113 


1.6 


20 


3.2 


168 


2.6 


188 


2.7 


60 


9.6 


304 


4.8 


364 


5.2 


11 


1.8 


74 


1.2 


85 


1.2 


24 


3.8 


423 


6.6 


447 


6,4 


27 


4.3 


242 


3.S 


269 


3.9 





0,0 


2 


0.0 


2 


0.0 


56 


8.9 


70 


1.1 


126 


1.8 


17 


2.7 


2C8 


3.3 


225 


3.2 


1 


0.2 


7 


0.1 


8 


0.1 


81 


12,9 


248 


3.9 


329 


4.7 





0.0 





0.0 





0.0 


150 


23.5 


450 


6.8 


580 


8.3 


275 


43.8 


1096 


17.2 


1371 


19.6 



328 



52.3 



1769 



27.8 



1097 



30.0 



MRFIT Study, Unpublished Data. 



544 



150 

1A0 

^ 130- 
en 

X 

I 120 

T 110 

zs 

S 100-1 
a 

"8 90 
o 

° 80 
70-1 
60 



TABLE 55 
Males 




..o 



Systolic 



...o 



:7-°" 




Urban •- 
Rural O' 



I I I I I I I I * 

15- 20- 25- »- 35- ^0- A5- 50- 55- 
Age in years 

Mean systolic and diastolic "blood pressure of 
urban and rural males. 



160 



150 



KO 

en 

X 130 
E 

1 120 



5 110 -I 
«/« 

°- 100 

CO 

80 -I 

70 

60 



Females 




o 




.-.-0 



Rural ©■ 
I I 



15- 20- 25- 30- 35- AO- 45- 50- 55- 
Age in years 

Mean systolic and diastolic blood pressure of 
urban and rural females. 

Oviasu VO, Okupa FE. Occupational factors in hypertension 
in the Nigerian African. J Epidemiol Community Health 19 79; 
33:274-278, 



545 



TABLE 56 



I <,15»/ < Mmm. Hg 

fig] 160-179/9S-109 
> 1 80/ > 1 10 




WM 



WW 



Risk of stroke or ischemic heart dis- 
ease according to blood pressure on entry-age- 
adjusied. In this figure and in the subsequent 
ones the numbers mthin each bar indicate the 
population at risk in the denominator and the 
subjects developing either stroke or ischemic 
^>'>i>rt disease in the numerator. 



Heyman A, Karp HR, Heyden S, et al: Cerebrovascular Disease in the 
Biracial Population of Evans County, Georgia. Arch Intern Med 1971; 
128:949-955. 



546 



TABLE 57 



Total F«lal and NofHatal SirokM* 








Fatal 


MontatX 


Total 1 


Group 


*— ** 


• SUat 


•too* 


•• 


•«n* 


•• 


Stroh 


aa 


8C 


mc 


ac 


ttC 


•C 


NC 


«C 


»IC 


Btaok man 


1,064(42) 


1.084(70) 




14 


26 


2« 


33 


40 


Bl«ak MMiwn 


1.344(04) 


1.364(81) 




la 


IS 


27 


34 


46 


WhHa in«n 


1. 802(80) 


1.801(130) 




12 


18 


36 


27 


47 




1.186(89) 


1.168(134) 




8 


14 


la 


IS 


20 


Total blacks 


2.408(8«) 


2.438(181) 


16 


32 


41 


63 


60 


00 


Total wttttma 


3.077 (I4S) 


3.017(264) 


14 


20 


32 


S3 


40 


73 


ToUJ 


6,4SS(348) 


6,466(416) 


2fl 


63 


73 


100 


103 


160 



*Oala lor 8lap(>«<l Car* (SC) and Ratanad Cam (RC) partlolpanla during 
raca-aax greupa. 

tNufli6ara M paranthaaaa Indtaala unknoona In a>tMm nontalal 
satafiMnafl. 



IOMOV.UP. by 
«as not 



Five-Year Findings of the Hypertension Detection and Follow-up 
Program. III. Reduction in Stroke Incidence Among Persons 
with High Blood Pressure. JAMA 1982;247:633-638. 



547 



TABLE 58 



Kumber of Deaths by Cause for MRFIT Black and White Men 



Cause of Death 
(TCP 9th Revision) 





Black Me 


a 




White Men 




No. 


Rate/ 
1000 


+ 
Percent 


Ho, 


Rate/ 
1000 


+ 
Percent 


450 


19.2 


100.0 


4602 


14.1 


100.0 


203 


8.6 


45.1 


2226 


6.8 


48.4 


30 


1.3 


6.7 


152 


0.5 


3.3 


78 


3.3 


17.3 


1225 


3.8 


26.6 


29 


1.2 


6.4 


483 


1.5 


10.5 


17 


0.7 


3.8 


26 


0.1 


0.6 


1 


0.0 


0.2 


7 


0.0 


0.1 


48 


2.0 


10.7 


333 


1.0 


7.2 



Total With Death Certificates 

All Cardiovascular Diseases 

Cerebrovascular Diseases 
(«30-438) 

Myocardial Infarction (410) 

Other Ischemic Heart 
Disease (411-414) 

Hypertensive Heart Disease 
(402) 

Other Hypertensive Disease 
(401,403-405) 

Other Cardiovascular Disease 
(390-459 Exclusive of 
above ) 

All Non-cardiovascular Diseases 247 

Genitourinary Diseases 

(580-629) 

Diabetes Mellitus (250) 5 

Neoplastic Diseases (140-239) 128 

Gastrointestinal Diseases 15 
(520-579) 

Respiratory Diseases (460-519) 12 

Infectious Diseases (001-139) 4 

Accidents, Suicides and 63 
Homicides (800-999) 

Other Disease 20 0.9 4.4 135 0.4 2.9 

+ Percent of total number of deaths in race group. 

Neaton JD, Kuller LH, Wentworth D: Total and Cardiovascular 
Mortality in Relation to Cigarette Smoking, Serum Cholesterol 

WMcrM"n"/oU»eVfYear"r """^ ^' "^"" *"°"^ "^'"^ =>"" 

548 



10.5 


54.9 


2376 


7.3 


51.6 


0.0 


0.0 


14 


0.0 


0.3 


0.2 


1.1 


37 


0.1 


0.8 


5.4 


28.4 


1440 


4.4 


31.3 


0.6 


3.3 


155 


0.5 


3.4 


0.5 


2.7 


124 


0.4 


2.7 


0.2 


0.9 


16 


0.0 


0.3 


2.7 


14.0 


455 


1.4 


9.9 



M 

m 




Oi <N 
^ CO 

rC CO 
(O 



s^ ■'sr 



CO '- 

o to 



(O 



IT) T- 

lo in 

0» CO 

co't-" 

CO 



o ^ 



(pejsnfpv-aBv) 000 L J3cl atey meeQ 
esBasiQ JBinosBAOjqejeo J^ax 9 



•<ir CM 
CO T 

r* CNj 

co" lo 

(O 



ca CO 
o '- 
CO •* 

CO* f^* 
(O 

II 

m » 



QJ 


C 


■u 


(U 


4-1 


S 


0) 




&^ 


<u 


« 


4-1 


00 -H 


•H 


£ 


u 


s 


o 


13 


4-1 


C 




CO 


c 




o 


Ai 


•H 


O 


4-1 


CO 


Cfl 


tH 


M 


CQ 


(1) 




oi 


00 




C 


c 





•H 




>, 




W 


01 


•H 


>-i 


rH 


3 


CO 


cn 


J-i 


en 


Vj 


01 


O 


u 


S 


Cl, 


Vj 


X) 


C3 


o 


1— 1 


o 


3 


rH 


u 


M 


en 




CO 


CJ 


> 


•H 


o 


rH 


•H 


O 


'O 


4.1 


Si 


cn 


CO 


CO 


u 


■H 




o 


T3 




"C 


X) 


CO 


c 




CO 


.—1 




CO 


c 


4-1 


o 


O 


•H 


H 


4-1 




CO 




J-i 


• ■ 


4-1 


Q 


C 




0) 


x: 


u 


u 


c 


u 


o 


o 


CJ 


S 




4-1 


rH 


C 


O 


<u 


!-i 


13 


CU 




U 


« 


cn 


X 


0) • 


J 


-H cn 




o u 


!-l 


^ CO 


OJ 


l; cu 


iH 


>< 


rH 


B 


3 


3 OJ 


^ 


Vj > 




0) -H 


•> CO fa 


Q 




■-l 


"T3 




00 0) 


c 


C 3 


O • 


H O 


4-1 ^ T— 1 


CO 


rH 


0) 


e 


2 CO [i, 



549 



Table 60 

Comparison of Logistic Regression Coefficients* For Diastolic Blood 
Pressure For All Cause and Cause Specific Mortality for Each Race Group 







Black 


Whit 


:e 


Difference 
In Coeff 






Coeff 


SE 


Coeff 


SE 


SE 


All Cause 
Mortality 


(1) 
(2) 


.0195 
.0202 


.0033 
.0035 


.0170 
.0171 


.0013 
.0013 


.0025 
.0031 


.0035 
.0037 


CVD Death 


(1) 


,0261 


.0051 


,0301 


.0019 


-.0040 


.0054 




(2) 


.0299 


.0055 


.0322 


.0020 


-.0023 


.0058 


CUD Death 


(1) 


.0188 


.0072 


.0263 


.0021 


-,0075 


.0075 




(2) 


.0244 


.0078 


.0289 


.0024 


-.0045 


.0082 


Death From 

Cerebrovascular 

Disease 


(1) 
(2) 


.0623 
.0624 


.0105 
.0109 


.0372 
.0324 


.0068 
.0072 


.0251* 
.0300* 


.0125 
,0131 



(1) All Participants in Race Group. 

(2) Excludes Those Participants Who Reported Previous Hospitalization 
for a Heart Attack or Taking Medication for Diabetes. 

* Estimated for Fixed Age, Serum Cholesterol and Cigarettes per Day. 

* P < ,05 

Neaton JD, Kuller LH, Wentworth D: To^l and Cardiovascular 
Mortality in Relation to Cigarette Smoking, Serum Cholesterol 
Concentration, and Diastolic Blood Pressure Among Black and 
White Men Followed 5 Years. 



550 



TABLE 61 



110- 
80- 
70- 
SO- 

30 - 



S 10 



70 



SO 



30 






M 



Strok* 



] No ECG Atinonnality 
j ECG Abnormality 






■ 



10 
277 



m 



e li 



Ha«n Diseaw 



" 14 



MM 



11 

10 10 
>73 J06 



WM WW BM BW I 

Ftisk of stroke or ischemic heart dis- 
ease according to ECG abnormalities on en- 
try—age-adjusted. 

Heyman A, Karp HR, Heyden S, et al: Cerebrovascular Disease in the 
Biracial Population of Evans County, Georgia. Arch Intern Med 1971; 
128:949-955. 



551 



TAULE bZ 



Five year mortality per 1000 in the absence of ECG abnormalities: HDFP participants with entry DBP of 9u ,o 104 mm 
Hg who were not on antihypertensive medication and were free of specific end organ damage at baseline* 





White 


men 


White y 


A'omen 


Black 


men 


Black 


women 


Total 




sc 


RC 


SC 


RC 


■SC 


RC 


SC 


RC 


SC 


RC 


Sample size (n) 
No. of deaths 


777 


745 


401 


408 


189 


169 


237 


284 


1604 


1606 


All causes 
CVD 
CHD 
Mortality rate 


22 

11 

8 


29 
12 
11 


12 
5 
3 


14 
4 
4 


14 
4 
3 


17 
6 
5 


6 
2 
2 


16 

11 

5 


54 
22 
16 


76 
33 
25 


All causes 
CVD 
CHD 
95% Confidence 


28.3 
14.2 
10.3 


38.9 
16.1 
14.8 


29.9 

12.5 

7.5 


34.3 
9.8 
9.8 


74.1 
21.2 
15.9 


100.6 
35.5 
29.6 


25.3 
8.4 
8.4 


56.3 
38.7 
17.6 


33.7 
13.7 
10.0 


47.3 
20.5 
15.6 


intervals for 






















(SC-RC) rate 






















All causes 

CVD 

CHD 


(-28.7, 
(-14.2. 
(-15.7, 


7.5) 

10.3) 

6.7) 


(-28.7, 
(-11.8, 
(-15.1, 


19.9) 
17.1) 
10.4) 


(-85.3, 
(-49.0, 
(-44.9. 


32.2) 
20.3) 
17.4) 


(-64.5, 
(-55.6, 
(-28.4. 


2.4) 
-5.0) 
10. 1) 


(-27.3, 
(-15.8. 
(-13.4, 


0.0) 
2.1) 
2.2) 



CHD = coronary heart disease; CVD = cardiovascular disease; SC = stepped care; RC = referred care 
'End organ damage includes history of definite myocardial infarction, stroke, intermittent claudication, angina pectoris or 
elevated serum creatinine (s|.70 mg/dl). 

Five year mortality per 1000 io the presence of ECG abnormalities: HDFP participants with entry DBP of 90 to 104 mm 
Hg who were not on antihypertensive medication and were free of specific end organ damage at baseline'^ 





White 


men 


White women 


Black 


men 


Black women 


Total 




SC 


RC 


SC 


RC 


SC 


RC 


SC 


RC 


SC 


RC 


Sample size (n) 


313 


318 


168 


198 


232 


298 


220 


216 


933 


1030 


No. of deaths 






















All causes 


21 


23 


7 


II 


18 


28 


8 


16 


54 


78 


CVD 


14 


12 


3 


8 


4 


15 


5 


5 


26 


40 


CHD 


11 


7 


2 


2 


4 


8 


3 


1 


20 


18 


Mortality rate 






















All causes 


67.1 


72.3 


41.7 


55.6 


77.6 


94.0 


36.4 


74.1 


57.9 


75.7 


CVD 


44.7 


37.7 


17.9 


40.4 


17.2 


50.3 


22.7 


23.1 


27.9 


38.8 


CHD 


35.1 


22.0 


11.9 


10.1 


17.2 


26.8 


13.6 


4.6 


21.4 


17.5 


95% Confidence 






















intervals for 






















(SC-RC) rates 






















All causes 


(-45.0. 


34.5) 


(-57.8, 


30.1) 


(-64.1. 


31.4) 


(-80.5. 


5.1) 


(-39.9. 


4.2) 


CVD 


(-24.0, 


38.0) 


(-56.5, 


11.4) 


(-63.0. 


-3.1) 


(-28.5. 


27.7) 


(-26.8, 


4.9) 


CHD 


(-12.9, 


39.1) 


(-19.7. 


23.3) 


(-34.5. 


15.2) 


(-8.8. 


26.8) 


(-8.3. 


16.2) 



CHD = coronary heart disease; CVD = cardiovascular disease; SC = stepped care; RC = referred care. 
*End organ damage includes history of definite myocardial infarction, stroke, intermittent claudication, angina pectoris, or 
elevated serum creatinine (2:1.70 mg/dl). 

The Hypertension Detection and Follow-up Program Cooperative 
Research Group. The effect of antihypertensive drug treatment 
on mortality in the presence of resting electrocardiographic 
abnormalities at baseline: The HDFP experience. Circulation 
1984;70:996-1003. 

552 



TABLE 63 



Five-year mortality rates in black and white males by education and presence of LVH at baseline for all 
HDFP stratum I participants and those not receiving medication at baseline: Referred-care males ages 40 to 69 years, 
with entry diastolic blood pressure of 90 to 104 mm Hg* 

<;;. Mortality 



(Deaths) N Crude Age-adjusted-f 



LVH-t l'VH+ LVH- LVH+ LVH- LVH+ 



All stratum I participants 

WM > HS (18) 446 (1)8 4.0 12.5 4.5 10.2 

WM = HS - (26) 402 ( 2) 10 6.5 20.0 7.0 21.9 

WM < HS (42) 335 ( 7) 16 12.5 43.8 10.6 28.6 

BM<HS (56)344 (11)32 16.3 34.4 15.4 32.3 

Participants not receiving medication at baseline 

WM > HS (13) 347 (1)8 3.8 12.5 4.4 10.2 

WM»HS (21)315 (0) 7 6.7 0.0 7.4 0.0 

WM < HS (22) 260 ( 5) 12 8.5 41.7 7.2 12.4 

BM<HS (41)268 (6)18 15.3 33.3 14.9 33.2 



WM - White males; BM - black males; HS - high school education completed. 

•From Tyroler HA: Race, education, and 5-year morulily in HDFP stratum I referred-care males. In Gross F. Strasser T, editors: Mild hypertension: 

Recent advances. New York, 1983, Raven Press. 

tAge-adjusted rates by direct method. Standard pupuUliun is age decade dUtribution of all white males aged 40 to 69 years with entry diastolic blood 

pressure of 90 to 104 mm Hg. 

tLVH determined by ECG. LVH+ defined as major LVH by Minnesota Code; LVH- defined as all others. 

Tyroler HA: (Overview of risk factors for coronary 
heart disease in black populations. Am Heart J 
1984;108:658-660. 



553 



TABLE 64 



STROKE INCIDENCE 



6r 



< 

tu 

o 
o 
o 



o 

HI -^ 
Q 

o 

z 



I I THROMBO-EMBOLJC 
■■ HEMORRHAGIC 



ii 



ill 



<\2\ 122-134 135-149 150+ 

SYSTOLIC BLOOD PRESSURE (mmHg) 
Incidence of stroke by quartile of systolic blood 
pressure. 

Kagan A, Popper JS, Rhoads GG: - Factors Related to Stroke 
Incidence in Hawaii Japanese Men. The Honolulu Heart 
Study. Stroke 1980;11:14-21. 



554 



TABLE 65 



ICM 




Tir 




<170 



I lo- 
ut 



J*»*N n 1 JJO 

MAMAII ]( } )j , 



140- 

159 



27 » 



■.4. 



160- iao» <i2o iro- 

"9 139 

SVSTOLIC BI.O00l>H€SSUnE ImnHfl 



I9« 



I ga- 
in 



13.1 



StatflttcaJ i*M tor lMM«( if«n4 
• * •P<0OS Sv« aos<:p<oio 

15 Hi r > 10 



Reluiiw risk of iiiinuntiiiiil hem- 
nrrlmin' und llinimhotmholw stroke hv syslolic 
blood pressure and counlry. 



Takeya Y, Popper JS , et al: Epidemiologic Studies of Coronary 
Heart Disease and Stroke in Japanese Men Living in Japan, Hawaii 
and California: Incidence of Stroke in Japan and Hawaii. 
Stroke 1984;15:15-23. 



555 



w 

H 



00 




















00 00 OS 


• 


3 






BS 


CN ^' 


<N 


»-i 












(U 












> 




Q 








O 




5: 


• 




cN r- tt 


en 


TS 

c 












IS3 












^r» 




















V^ (N vo 


<r> 










00 ^ 


w-> 


•T3 




<N r- o\ 


ON 


bO 


^ 


f2 




f^ <N -^ 


r^ 


C/5 












a 












o 








vq tN 00 


00 


2 






b^ 


C> fS 00 


^ 


S.^ 












■tad 




Q 












^ 


• 


^-« »0 CO 


Tf 








Tf en 


00 


t^ 4) 


u 










r. ^ 


""* 






(N ro 00 


cn 


U 3 


6 






00 <N 


^^ 






<N VO <N 


^* 




f2 




r- ^ ^ 





cd CU 












1> «-• 












■— o 












•O § 
























ular 
ofb 








<N SO -M 


p 






^ 


• • • 

^ cn r- 


en 


u .^ 












52 <u 












5 > 




n 








oii 






• 




-^ <N VO 


ON 








r- '^ <N 




1-4 












D O 












from c 
rding t 


Jh 


"5 




<r\ <ys 00 





'c3 


-<->• 




<N r- m 


Tt 


2 


s2 




On -^ r^ 


00 












^ o 












>^ O 












-3 cd 












•^ _- 












1- -o 








u 




Mor 
erio 












a. 








irmotei 
rderlin 
perten 




b!e3. 

year 










h2 








:2; m K 


e2 



M 




OJ 




3 




J= 




• m 




C 1) 




CO -H 




s > 




•H 




to • 




H rc 




c •> 




•H tl 




M 




0) 3 




^ (0 




c 




H 0) 




•u en 




m 




T) pi 




c 




cd " 




)-i 




C 0) 




en 




•H CO 




en CO 




C hJ 




OJ 




U ' 




u p 




(U 




0. ' 




?^ OC 


• 


^ c 


m 


•H 


00 


M-< A! 


CT\ 


CO 


.— 1 


S 




>> 


#» 


■a 0) 


c 


3 x: 


•H 


U U 


iH 


in 


l-i 


c 


CU 


rH -H 


n 


CO 




U HI 


A 


•H S-1 


tJO 


00 CO 


CO 


U 


tH 


iH 


)-i 


j: 


<U 


•H -U 


> 


e -H 


1 


(U CO 


u 


X) 0) 


0) 


•H p5 


00 


CX 


c 


W >- 


•H 


>-j 


)-i 


CO 


0. 


• 6 


Cfl 


Oh -H 




:s „^ 


•* 



PL, 

00 

C CO 

0) .. 73 

cn C OJ 



556 



TABLE 67 




r^isk Of Stroke or ischemic heart 
disease according to level of serum cho- 
lesterol on entry— age-adjusted. 

Heyman A, Karp HP.; Heyden S, et al: Cerebrovascular Disease in the 
Biracial Population of Evans County, Georgia. Arch Intern Med 1971; 
128:949-955. 



557 



00 

W 



c 


c 


<u 


03 


5 


2 


ji£ 


(0 


o 




CO 


JT 


CD 


$ 


• 






lO 



CO 




^ 
^ 


rs. o 


«r 


r». <o 


^ 


CO <N 


4. 


^ r>^ 




<o 



TT to 

CO 



or N- 
cvj c\» 

CO 



(p9^snrpv-96v) 000 1 J8d 9jBa Mieaa 

3SB3S!a JB|n0SBA0jqaJ9Q JB3A 9 



IT) CO 
CO cvi 
CO CNJ_ 

^ in 

CO 



CT)_CO_ 

CO 

c c 

s $ 

d 6 
z z 



C (1) 

o u 

•H 3 

■u tn 

tfl M 
iH OJ 
OJ u 

Oi PU 

C T3 

•H O 

o 
>. t-l 

U P3 

■H 

rH O 

■u ^ 
1-1 o 

O 4J 

S tn 
CO 

U •r^ 

ta Q 

O C 

en CO 
CO 

c 
o 

•H 
u 
CO 
Vi 
u 

a 

o 

c 
o 



> 

o 

•H 
13 
U 
CO 

T3 
C 
CO 



O 
H 






cn T3 

0) <1) 



J= o 

■u x: 

u u 
o 



o 



o 



C Vj C3 

<U (U CU 

s M> a 

•H jr 
0) o 



3 



S -d 



cu 



CO 



CO 



0) CO 

CO « 

bO 
60 
C 
O 

O 6 



558 



TABLE 69 

Comparison of Logistic Regression Coefficients'*' For 

Serum Cholesterol Concentration For all Cause and Cause Specific 

Mortaliltj For Each Race Group 







Blj 


ick 


Whit 


:e 


Difference 
In Coeff 






Coeff 


SE 


Coeff 


SE 


SE 


All Cause 
Mortality 


(1) 
(2) 


.0016 
.0013 


.0010 
.0011 


.0028 
.0024 


.0003 
.0004 


-.0012 
-.0011 


.0010 
.0011 


CVD Death 


(1) 


.0054 


.0014 


.0072 


.0004 


-.0018 


.0014 


- 


(2) 


.0059 


.0015 


.0073 


.0005 


-.0014 


.0015 


CHD Death 


(1) 


.0071 


.0017 


.0079 


.0005 


-.0008 


.0018 




(2) 


.0079 


.0017 


.0082 


.0005 


-.0003 


.0018 


Death From 

Cerebrovascular 

Disease 


(1) 
(2) 


-.0034 
-.0032 


.0046 
.0047 


.0023 
.0021 


.0020 
.0021 


-.0057 
-.0053 


.0050 
.0051 



(1) All Participants in Race Group 

(2) Excludes Those Participants who Reported Previous Hospitalization 
for a Heart Attack or Taking Medication for Diabetes. 

•f Estimated for Fixed Age, Diastolic Blood Pressure and Cigarettes 
per Day 



Neaton JD,_Kuller LH, Wentworth D: Total and Cardiovascular 

Mortality m Relation to Cigarette Smoking, Serum Cholesterol 

Concen ration and Diastolic Blood Press^^re Among Black and 
White Men Followed '^ YpaT-= ^ 



559 



TABLE /O 



6r 



a. 
< 

ai 

>- 

o 
o 
o 



UJ 

o 

z 

Q 

o 



STROKE INCIDENCE 



I ) TMROMBO-EMBOUC 
Hi HEMORRHAGIC 




< 193 194-216 217-241 



242+ 



CHOLESTEROL ( mg /dl ) 
Figure 7. Incidence of stroke by quartile of serum 
iholeslcrol. 

Kagan A, Popper JS, Rhoads GG: Factors Related to Stroke 
Incidence in Hawaii Japanese Men. The Honolulu Heart 
Study. Stroke 1980;11:14-21. 



560 



TABLE 71 



Cerebral Hemorrhage* 



10 

OE 


3- 




















> 


2- 




2.53 
















1.98 






o 










•a 

01 


1 - 
0- 












0.35 
1 1 


0.89 




TJ 




0.63 














ni 










130 160 


200 


230 




\ 1 1 


1 










129 




159 




199 


229 







Serum Cholesterol (mg/IOOml) 



Cerebral Infarction 



QC 

> 

o 



re 
■O 

c 

ni 

«-» 



3- 
2- 
1 - 
0- 



1.43 



i 
129 



130 

? 
159 



Standardized morbidity ratio for 
stroke by the level of serum cholesterol at entry 
(both sexes. S 40 years of age at entry, lO-year 
follow-up. Taisho, Japan}. 







1.04 




1.00 




1.12 








0.59 

















160 

) 
199 



200 
229 



230 



Serum Cholesterol (mg/100ml) 

• The decreasing trend (slope) is significantly different 
from zero at the p < 0.05 level. 

Tanaka H, Ueda Y, Hayashi M, et al: Risk factors for cerebral 
hemorrhage and cerebral infarction in a Japanese rural 
community. Stroke 1983;13(1) :62-73. 



561 



TABLE 72 



/l.V<'-"'//'<»'<'</* .W<<//i» (ij Si'liiinl Variiihici uiili uiul \tlihe^l Stroke — Diti'iiir 


llllll Pt'wihlc C(/M\ 


Japan 


Hawaii 


Non- Nim- 
Vuriablc iirukc ICH T-E slrokc 


ICH T-V. 



SysUdic MihkJ prcvsuro (mm Hi:) 135. 2 163.4**"' 

Dia>Uilic blAKJ prcs.sure (mm Hg) 84.4 97.2** 

Scrum chulcMcrol (mg/IUil inO I9U.8 IK3.7 

Hcmalinrrit (C5( 43.3 44.2 

Relative lH)dy weight (Cf) 101. 7 I0«.7 

Cisareite/Uay 13.7 10.3 

Calorie 2251 2144 

Animal protein (g) 42.2 28. 1 

Vegetable protein (g» 38.0 44.7 

Saturated fai(g) 17.7 10.9 

Unsaturated I'al (g) 22.1 20.7 

Simple carbohydrate (g) 63.0 67.0 

Complex carbohydrate (g) 283.9 270.0 

Alcohol (g) 31.1 40.6 

Calorics 'body weight (kg) 41.0 .38.0 



161 4^" 
IS«6 

44i 

Iii77 

20.>w Sug 

36. S 
9 0' 

l'J4 

2SI ; 

24 7 



I3S.K 
SI. 9 

217.1 
44.5 

111.8 
9.6 
2177 
66.9 
23.3 
55. 1 
24.5 
86.9 

166.7 
12.2 
35.6 



148. y^^* 

2(>7.4 Sug 

44.2 
115.8 

12.1 
2020 

54.3" 

24.9 

4I.I**» 

29.6 

74.1 
170.9 

13.0 

31.8 



154.1*"^ 

88.8**'* 
218.5 

44,6 
III.7 

11.7 
2063 

57.4*- 

21.9 

53.3 

20.7* 

86.4 
159.0 

14.2 

33.7 



^Age adju.Ntmcnl con.stanis 
Japan 
45-54 0.216 
55-59 0.267 
60-64 0.262 
65-69 0.255 
Sug.: ;j< 0.10 
*: i> < 0.05 
•*: /» < 0.01 
•••: p < 0.001 



Hawaii 
45-49 0.120 



50-54 
55-59 
60-64 
65-69 



0.233 
0.211 
0.256 
0.180 



Heart V' ^°PP^"/f ' ^' ^^'- Epidemiologic Studies of Coronary 



562 



TABLE 73 



SliiiiiJiirJiirtl Muhifilf hii;hlir Fuiuiitm CiH-ffiiiciils — Ocjiiiiic ami Piiwihic Slrnke Ciisfs 







SlanJardi/ed ciKllicicnl 


Absolute 


CDcHicieni 




Variable 




Japan 


Hawaii 


Japan 


Hawaii 


TcMt 


Syslolic hliKHl pressure (mm 


Hgl 


0.73» 


0.45* 


0.030 


0.021 


NS 


Scrum cholesterol (mti/KH) ml) 


-0.12 


-0.06 


- 0.(X)3 


-().(X)2 


NS 


Relalivc boily weight (C< ) 




-0.01 


-0.12 


-0.001 


-0.(K)l 


NS 


Hcmuiocrii {'^) 




0.24 Sug. 


-0.06 


0.066 


-0.019 


NS 


Proteinuria 




0.19 Sug. 


0.14* 


0.384 


1.046 


NS 


LVH in IdCG 




-0.08 


0.26* 


-0.401 


0.880 


• 


Alcohol (g) 




-0.11 


0.12 


-0.002 


0.005 


NS 


SjluralcJ Tat (g) 




-0.22 


0.02 


-0.041 


0.002 


NS 


Animal protein (g) 




-0.27 Sug. 


-0.27* 


-0.077 


-0,062 


NS 


Cigarettes per day 




" 0.14 


-0.12 


0.012 


0.009 


NS 


Calorics/body weight (kg) 




-0.22 


-0.I7' 


-0.019 


-0.013 


NS 


Age 




0.39* 


0.30* 


0.069 


0.053 


NS 


+Tcsts for Uifferencc of absolute cocfficicnr between 

NS:p > 0.10 

Sug.:/7 < 0.10 

*:p< 0.05 


two countries 









Takeya Y, Popper JS, et al: Epidemiologic Studies of Coronary 
Heart Disease and Stroke in Japanese Men Living in Japan„ Hawaii 
and California: Incidence of Stroke in Japan and Hawaii. 
Stroke 1984;15:15-23. 



563 





TABLE 


74A 




CA'.V Dis,,is,' 


y.\. \o CVS Diwaw ai A, 


UlOftW 




Agi 


.' adjusted moans 




No 

disease 

(191) 


Brain 
iiffarilion 


Hcinnnha^'C 


llxiiminaiiim variables 








BMI («i/hl-) 


23.5 


24.5 


23.7 


Cigarciics/day 
Scrum cholesterol 


12.9 
216 


11.7 
235+ 


19.8' 
202 


Scrum Iriglyccridc 


246 


220 


214 


Serum uric acid 


6.2 


6.1 


6.7 


1-hr. pp. glucose 


178 


199 


156 


HcmuKKril 


44.7 


45.8* 


44.1 


FVC 


3.1 


2.93 


3.29 


Systolic BP 
Diastolic BP 


1.39 
83 


146 

87* 


153* 

95$ 


Diet variables 








Calories 


2311 


2032* 


2322 


Alcohol (g/d) 


20.3 


13.5 


29.1 


Animal prvicin (g) 
Vegetable protein (g) 
Saturated fat (g) 


69.4 
23.0 
59.6 


67.7 
20.4 

53.3 


.59.6 

22.7 
51.2 


Unsaturated fat (g) 
Starch (g) 


23.9 
167 


23.5 
1.36* 


27.9 
14« 


Cholesterol (mg) 


565 


512 


463 


■^ Calories, protein 


16.2 


17.7* 


14.9 


'k Calorics, fat 


32.6 


.33.3 


.'0.6 


<> Calories. CHO 


45.1 


45.0 


46.2 


■* Calorics, alcohol 


5.3 


3.97 


7.9 


Sodium 


.1011 


2520 


2558 


Autopsy variables 








Age at death 


63 


67 


62 


MI(^) 


34.3 


.'58.5+ 


18.2 


Heart weight 


374 


412* 


395 


Aorta score 


3.94 


4.54+ 


4.12 


Coronary score 
Circle of Willis score 


3.05 
0.82 


4.09* 
1.37* 


3.24 
1.41* 



*p « 0.05. +p S 0.01. i/» « 0.001. Significance tests arc 
based on the contrast to the no disease group. 

Stemmermann GN, Hayashi T, Resch JA, et al: Risk Factors 
Related to Ischemic and Hemorrhagic Cerebrovascular Disease 
at Autopsy: The Honolulu Heart Study. Stroke 1984;15:23-28. 



564 



TABLE 74B 



<"A'.S l)(\€-ii\f y\ All /.Midi'. .U'«'-«<</;;/,\7<i/ Mmm 





All 


Brain 






livini! 


inlari'lion 


Honiiirrhaac 




(07531 


(57) 


(22) 


Exjminuiion vuriuhlcs 








Bixly mass index 


23.9 


24.5 


23.8 


Cigareucs/'day 


9.7 


12.4 


20.. 5+ 


Scrum iliolcMcrol 


:iK 


233-J- 


202* 


Scrum uijilyccride 


2M 


237 


221 


Uric acid 


5.96 


6.15 


6.7«t 


Glucose 


I5R 


l%i; 


I.S3 


Hcmaiocrit (<J) 


44.7 


46.0> 


44.3 


FVC 


.V25 


2.99? 


3.. ^6 


Systolic BP 


1.^3 


l44Ji 


1.52ii 


Diastolic BP 


82 


87t 


95§ 


Diet variables 








Calories 


2301 


2091* 


2394 


Diet alcohol (g/d) 


12.9 


13.8 


29.9t 


Animal protein 


71.6 


70.1 


62.4 


Vegetable protein 


23.7 


20.4* 


22.9 


Saturated fat 


60.1 


56.3 


54.2 


Unsaturated fat 


26.5 


23.7 


28.7 


Surch 


164 


139t 


1.50 


Sugar 


46.1 


38.4 


.'i2.2 


Cholesterol 


549 


537 


478 


CI Calorics, protein 


16.7 


17.7 


14.9* 


% Calories, fat 


33.5 


34 


31.2 


rt Calories. CHO 


46.3 


44.3 


45.5 


•J Calorics, alcohol 


3.57 


3.94 


7.98t 


Sodium 


2914 


2586 


2646 



'p ^ 0.05. +/J « 0.01. i/> « O.OJI. S/J ^ 0.0001. Signifi- 
cance tests are based on The contrast to the living group. 

Stemmermann GN, Hayashi T, Resch JA, et al: Risk Factors 
Related to Ischemic and Hemorrhagic Cerebrovascular Disease 
at Autopsy: The Honolulu Heart Study. Stroke 1984;15:23-28, 



565 



TABLE 75 



Percent of the United States population with diabetes ^ 1976-80* 

Age (Years) 



20-74 20-44 45-54 55-64 65-74 



White 6.2 1.7 8.2 11.9 16.9 

Male 5.3 1.0 7.7 9.1 18.1 

Female 7.0 2.2 8.5 14.5 16.1 

Black 9.6 3.1 12.9 20.8 25.9 

Male 8.5 2.8 11.1 14.4 29.4 

Female 10.5 3.5 14.5 25.4 23.1 

*Sum of percent of persons with a physician-diagnosed medical history of diabetes and of 
undiagnosed diabetes using NDDG criteria. 

SOURCE: Hadden, WC, and Ml Harris. Prevalence of diabetes and Impaired glucose tolerance and 
plasma glucose In the United States population. NCHS Vital and Health Statistics, 
Series 11, In preparation. 

Diabetes in America, Diabetes Data Compiled 1984. U.S. 
Department of Health and Human Services, NIH Publication 
No. 85-1468, August, 1985. 



566 



TABLE 76 



250r 



^2 SAVANNAH 













m 

i 
i 




— 







%i 

y,y/. 
■Ayy 
W 

i 



^^^ 



11 



p 



■ 



w 



WHITE 
MALES 



WHITE 
FEMALES 



BLACK 
MALES 



BLACK 
FEMALES 



R 

h. 



4 
m 



ALL 
GROUPS 



MeoA ehoiaierol aiui bhod gii^os* 
delerminations and 95% confidence limits I ± 1.96 
standard error) by color and sex for each city. 
1972-1974 



Stolley PD, Kuller LH, Nefzger MD, Tonascia S, et al: Three-Area 
Epidemiological Study of Geographic Differences in Stroke Mortality 
II. Results. Stroke 1977;8:551-557, 



567 



TABLE 77 



Oiobslat 
Median Vasiol Scores ol Given Aga 





40 




— 


NO OioMI«» -^ 




m 
o 


30 


» - 


-- 


OtflMttt "^ 




1 


20 
10 



■ 


IT 


,^ 


/^ 










^^ 



JO 40 30 60 70 80 90 



liediau veisel score* for diabetic and nondiabetic 
mdes and femdea. in the fifth and sixth decade* the 
diabetic female has higfter median vessel secret than 
even the diabetic male. 



Source: Ila, G.C. Flora, A.B. Bafcer, R.B. Loewenson and A.C. Klassen: 

A Comparative Study of Cerebral Atherosclerosis in Males and Females, 
Circulation , Volume XXXVIIT, November, 1968. 



568 



TABLE 78 



D»Mth Rat*» and Mortalltf Ratlot tor CHD and SUoka bf Hiatoty at Dlabmtas 
and High Blood Prtaun by Sau and Aga 





Age 
Group 




CHD 






StroKe 




Sex 


Neither 
Diabetes 
nor High 

Blood 
Pressure 


High 

Blood 

Pressure 

but not 
Diabetes 


Diabetes 

but not 

High 

Blood 

Pressure 


Both 
Diabetes 
and High 

Blood 
Pressure 


Neither 
Diabetes 
nor High 

Blood 
Pressure 


High 

Blood 

Pressure 

but not 

Diabetes 


Diabetes 

but not 

High 

Blood 

Pressure 


Both 
Diabetes 
and High 

Blood 
Pressure 












Death Ra 


tes 










40-49 


152 


423 


400 


1.078' 


17 


68 


*•• 


... 


M<?r\ 


50-59 


390 


910 


993 


1.995 


44 


227 


126 


■ ■• 




60-69 


803 


1,735 


1.950 


1.891 


163 


507 


258 


729» 




70-79 


1.788 


2.904 


3.090 


5.499 


604 


1.311 


839 


2.0U* 




40-49 


15 


81 


182» 




12 


72 






Vkonten 


50-59 


57 


196 


411 


550 


28 


91 


83 • 


... 




60-69 


228 


504 


1,095 


1,378 


86 


244 


320 


440 




70-79 


798 


1.397 


2.412 


2.650 


393 


737 


837 


779 












Mortality R 


alios 










40-49 


1.00 


2.78 


2.63 


7.09* 


1.00 


4.00 


• >■ 


... 


Men 


50-59 


1.00 


2.33 


2.55 


5.12 


1.00 


5.16 


2.86 


..• 




60-69 


1.00 


2.16 


2.43 


2.35 


1.00 


3.11 


1.58 


4.47* 




70-79 


1.00 


1.62 


1.73 


3.08 


1.00 


2.17 


1.39 


3.33» 




40-49 


1.00 


5.40 


12.13* 


• ■• 


1.00 


6.00 


• •■ 


... 


"kiirtL-n 


50-59 


1.00 


3.44 


7.21 


9.65 


1.00 


3.25 


2.96» 


... 




60-69 


1.00 


2.21 


4.B0 


6.04 


1.00 


2.84 


3.72 


5.12 




70-79 


1.00 


1.75 


3.02 


3.32 


1.00 


1.88 


2.13 


1.98 



' fiates based upon only five to nine daiths. 



Source: Illb, E.G. Hammond and L. Garfinkel: Coronary Heart Disease, Stroke, and 
Aortic Aneurysm. Arch. Environ. Health . Vol. 19, August, 1969. 



569 



TABLE 79 



210- 



ISO- 

uo- 

130- 

120H 

110- 



o 
o 
o 

2 100- 



< 



u 

z 



9 
a 



90- 
80- 
70- 
60- 
50- 

40- 

30- 
JO- 
10- 
0- 



I I AtSENT 
I PRESENT 



WOMEN 



i0i9 AO-49 70-79 



50-29 60-69 70-79 



AGE AT EXAM 

Average annual incidence of athero(hrombotic brain infarction according to 
diabetic status, age at biennial examination, and sex; 22-year toilow-up. Diabetes Is 
significantly associated witf) ABI Incidence, p < 0.05 in men and p < 0.001 in women. 



Source: Illb, P.A. Wolf, T.R. Dawber, H.E. Thomas, T. Colton 
and W.B. Kannel: Epidemiology of Stroke. Advances 
in Neurology, Vol. 16. 



570 



TABLE 80 



Niunbtr of deaths in which c«rebrova$exdar diuau was lisUd on tks death certificate and percent that 

also lisUd di<^Us, arUriosclerolic heart disease or hypertensive disease in Baltimore City and 

a counties in Maryland based on multiple-cause lobulation of death certificalee for iOeo* 















iMcek 

MS 


No. CVD OUiaaiii 




Pucwug* with byptf- " 
taBiivadixaM 


Pucattci wiU ASHQ 




Bklti- 
Bon 


Euum 


WnUn 


BtlU. 
oion 


EatUiD 


WMUrn 


BUU. 
man 


EutUB 


WctUm 


Btia- 
Bun 


EUUIB 


W«M«| 


WM 

WF 
NM 

NP 


321 
300 
164 
183 


lfi6 

164 

02 

68 


197 
200 


6.6 

0.8 

4.0 

10.0 


8.1 
11.0 

2.2 
14.1 


6.o: 

13.0 


27.0 
36.2 
38.7 
46.1 


21.0 
32.0 
26.6 
36.4 


26.6 
34.3 


33.6 
31.0 
23.7 
30.7 


21.3 
10.6 
18.1 
16.2 


18.6 
24.1 


Total 


967 


460 


406 





















• 1060, 1061, 1062 duAthit in oouati^a. 

t Excludes deaths due to cerebral aaeuryam. 



Source: Ua, L. ^-^^llXJe'asTllrllllty in Maryland. 

rprebrovascular Disease iiui-i.'* j Nn 2 

JournalofjEideioiolosx. Vol. 86, No. 2. 



American 



571 



TABLE 81 



Disiribufion of Of her Diseases Listed in Hospital Chart—Stroke Cases fay Area (Ages 45-69) 





Totol 
stroke cases 


Hypertension 


OiMoses 
ASHD 


Diabetes 


At 
least 
one 
No. 




Aiea 


No. 


% 


No. 


% 


No. 


% 


% 


Miami 


531 


159 


29.9 


206 


38.8 


91 


17.1 


289 




54.4 


Denver 


293 


81 


27.6 


91 


31.1 


36 


12.3 


135 




46.1 


Kansas 


130 


42 


32.3 


32 


24.6 


15 


11.5 


62 




47.7 


Seattle 


365 


90 


24.7 


82 


22.5 


44 


12.1 


142 




38.9 


Buffalo 


532 


224 


42.1 


237 


44.5 


143 


26.9 


348 




65.4 


North 






















Carolina 


214 


88 


41.1 


59 


27.6 


36 


16.8 


123 




57J 


Georgia 


93 


30 


32.3 


31 


33.3 


15 


16.1 


54 




58.1 


South 






















Carolina 


162 


37 


22.8 


13 


8.0 


8 


4.9 


37 




22.8 


Total 


2,320 


751 


32.4 


751 


32.4 


388 


16.7 


1,190 




51.3 



Excludes deaths certified by medical examiner (five), cases discharged alive from hospital but subsequently 
found dead in mortality study (40), and stroke on past history only. 



Source: lib 



I: S:ifeld.l!i:its;r!^Ha;io;»!rc:;e°;ov.scula/aisease Mo.Mdity Study. 
Stroke 1:86-99, 1970. 



572 



TABLE 82 



l-rcciuL-ni y uf First Stroke in the t)i.iliflic Ciihurt, RuLhcster, Minnrbuta, 194S-19b9* 



Paiienib 













^Jj ■,; 








Relative 




coniiiience 


Perbon-years 






risk 




intervals 


at risk 


Observed 


tA|jCLted . 


(obs/e.xp) 


P value 


01 ubs/exp 






Hypti tensive 








1,136 


22 


IU.7 


2.1 


<0.001 


1.3-3.1 


2,57(1 


36 


23. 5 


1.5 


<0.05 


1 1-2.1 


J, 712 


58 


14 2 
Noiilivpi-rtensive 


1.7 


<0.00l 


1.3-2.2 


4,2'J4 


34 


111.3 


1.1 


NS 


0.8-1.6 


3,172 


21 


17 7 


1.2 


NS 


0.7-1.8 


7,4(iii 


S'S 


1)1 


1.1 


NS 


0.9- 1 5 



Males 
Females 
Total 

Males 
Females 
Tui.il 



•Obi = observed; exp = ex|)eLled: NS = not siyiiilicant. 

Source: Ilia, M.E. Roehmholdt, P.J. Palumbo, J. P. Whisnant and L.R. Elveback: 

Transient Ischemic Attack and Stroke. Mayo Clin. Proc , Jan 1983, Vol. 58, 



573 



TABLE 83 



cc 
< 
tu 
>- 

o 
o 

o 



UJ 

o 

z 

UJ 

Q 



STROKE INCIDENCE 



6r 



I I THROMBO-EMBOUC 
■i HEMORRHAGIC 



Lil il il 



:S122 



122-149 150-188 189+ 
GLUCOSE (mg/dl) 

Incidence of stroke by quarlile of serum 
glucose I hour after a 50 gm oral load. 

Kagan A, Popper JS, Rhoads GG: Factors Related to Stroke 
Incidence in Hawaii Japanese Men. The Honolulu Heart 
Study. Stroke 1980;11:14-21. 



574 



TABLE 84 



Age-adjusted Death Rates per 1000 (in 9 years) 
by Level of Alcohol Consumption 



Alcohol 
(oz/mo) 


CHD 


Thrombo- 
embolic 
stroke 


Hemorrhagic 
stroke 





24.6 


3.7 


3.0 


1-6 


16.6 


5.2 


3.2 


7-15 


20.9 


3.0 


7.3 


16-39 


7.8 


1.8 


6.3 


40-59 


5.9 


3.7 


5.5 


60+ 


12.8 


5.1 


12.7 



Abbreviation: CHD = coronary heart disease. 



Kagan A, Yano K, Rhoads GG, et al. 
Alcohol and Cardiovascular Disease: 
The Hawaiian Experience. Circulation 
1981;64(Suppl III) :III-27-III-31 . 



575 



TABLE 85 



STROKE INCIDENCE 



6r 



< 
tu 
> 

o 
o 
o 



UJ 

o 

HI 2 

Q 

O 



s 



I I THROMBChEMBOUC 
■H HEMORRHAGIC 



Li 



\3L 



17 + 



1-16 

ALCOHOL CONSUMPTION (ml /day) 

Incidence of stroke by lertik' of alcohol con- 
sumption. 

Kagan A, Popper JS, Rhoads GG: Factors Related to Stroke 
Incidence in Hawaii Japanese Men. The Honolulu Heart 
Study. Stroke 1980;11:14-21. 



576 



vO 
GO 

w 
►J 
m 
< 




05 CO 
CO t». 
en csj 

CD 
CO 



to 


>. 


00 ■^ 


CJ 


(0 


CO ■^ 


1 
CO 


"a 


y- O 


N 


0) 

Q. 

■a 
o 


T-* r«-" 

CM 


«l> 


Q. 


LOOT 


CM 


0) 


OOJ 


1 
(O 


QC 


O)C0 




(0 


"«foo* 




o 


CO 




*« 






•>• 






0) 






k. 






(0 






O) 












b 




to 


*- 


O "><• 


o 


CO 00 


1 


, 


fx. '- 




o 

z 


CVJ 



0-± o 



(psjsnfpv-36v) 000 1 J^cl ajBy MiBaQ 
asBasjQ jBinosBAOjqsjao Jea^ 9 



CO *- 
«sr CO 

r-'oO* 

CM 

C C 

a o 
Z 2 

^ « 

u x: 

ffi i 

6 6 
z z 



c (U 




O M 




•H 3 




4J cn 




Cfl w 




rH 0) 




OJ l-l 




PS P^ 




C TJ 




•H O 




o 




>,M 




4-1 P3 




•H 




tH O 




CO -r-l 




4-1 t-i 




M O 




O 4-1 




S M 




cd 




l-l -H 




tfl Q 




iH 




D -a 




o C 




U5 CO 




CO 




> c 




o o 




•l-l -H 




ID 4-1 




U CO 




CO M 




U 4J 




C 


• 


•a <u 


cn 


C O 


l-l 


CO C 


CO 


o 


(U 


r^ U 


>-' 


CO 




4J rH 


(U 


o o 


?> 


H (-1 


•H 


01 


lil 


4-1 




.. tfl 


T) 


Q <U 


0) 


iH 


3 


^ O 


o 


W ^ 


rH 


u u 


iH 


o 


o 


3 e 


[in 


4-1 3 




C ^4 


c 


0) 0) 


<u 


S 00 


s 


A VI 


0) 


33 00 


4-1 


hJ c 


•H 


•H 


J= 


u ^ 


S 


OJ o 




r-l 6 


TS 


rH C/: 


c 


p 


to 


Srf 0) 




4-1 


.^ 


« iJ 


a 


Q (U 


to 


•-5 H 


iH 


CO 


m 


C M 




O -H 


00 


4-1 U 


c 


(0 


o 


OJ o 

2 4-1 


1 



577 



TABLE 87 



i 




\ 



Risk of stroke or ischemic disease 
according to level of hematocrit— age-ad- 
justed. 



Heyman A, Karp HR, Eeyden S, et al: Cerebrovascular Disease in the 

Biracial Population of Evans County, Georgia. Arch Intern Med 1971;128:949-955, 



4 



578 



TABLE 88 



DEFINITE THROMBO-EMBOLIC STROKE 



m HYPERTENSIVE 

1 I NOT HYPERTENSIVE 



QC 
< 

UJ 8 



o 
o 
o 



OJ 

o 

z 
111 

Q 
O 

z 



UJ 



4 
2^ 



? " . 

^^^ 




12 3+ 

NUMBER OF Rl$K FACTORS 



UJ 

O 

Q 
O 

I 2 + 

NUMBER OF OTHER RISK FACTORS 



* ; C4S£ OMITTED BECAUSE OF MISSING DATA 
Incidence of ihromboembolic stroke according to number of risk factors: 
hypertension (BP ^160/95): cigarette smoking: hyperglycemia (>170 mg/dl, I h after 50 gni 
glucose, p. 0.1. increased hematocrit ('k48%j: and/or left ventricular hypertrophy or strain on 
the ECG. Numbers within bars denote the number of cases. 

Kagan A, Popper JS, Rhoads GG: Factors Related to Stroke 
Incidence in Hawaii Japanese Men. The Honolulu Heart 
Study, Stroke 1980;11:14-21. 



579 



TABLE 89 



% 

30 



25 



20 



10 



5 - 



ZaHDFP 
■ IHI 



12.8 



I 




WHITE 
MALE 



255 



I 



?29 



WHITE 
FEMALE 



BLACK 
MALE 



198 



i 



m 



IGO 



BLACK 
FEMALE 



\ 



I 



\ 



\ 



Change in prevalence of elevated diastolic 
blood pressure: HDFP (1973-74) and IHI (1977-78) (DBF 
^ 95 mm Hg). 

Apostolides A, Cutter G. Kraus JF, et al: Impact of Hypertension 
Information on High Blood Pressure Control Between 197randT978 
Hypertension 1980;2:708-713. 



580 



TABLE 90 



Secular trends in hypertension control 



Study 



Date 



Per cent under control* 



Men 



Women 



Minnesota Heart Survey (10) 



Anglos 
1973-1974 



29% 



53% 



Hypertension Detection and 
Follow-up Program (23) 

Impact of Hypertension 
Information Study (8) 

Minnesota Heart Survey (10) 



1973-1974 

1977-1978 
1980-1981 



28% 



44% 



72% 



52% 



69% 



81% 



San Antonio Heart Study 



1979-1982 



87% 



97% 



Laredo Study (12) 

San Antonio Heart Study 



Mexican Americans 



1979 



1979-1982 



37% 
64% 



77% 



87% 



* Expressed as per cent of total hypertensives in the community, including both treated 
and untreated. 

These studies also present data on hypertension control in blacks which indicate that 
black women are better controlled than black men and that the level of control in the 
black community also improved from 1973-1974 to 1977-1978. 



Franco LJ, Stern MP, et al: Prevalence, Detection and Control of 
Hypertension in a Bi-Ethnic Community: The San Antonio Heart Study. 
Am J Epidemiol (In Press). 



581 



1-4 



>■ 

h- 

< 

o: 
O 

< 
UJ 

I 

Q 
2 
< 



m 

X 
U4 
Q 
Z 

CO 

(/I 
< 

> 

Q 
O 
OQ 
u 

2 

u 

CO 

< 

03 



c 

Q. 



a 



u 
T3 

t 
Cii 



c 

CO 

D. 



D. 



U 

I 
T3 

a. 

Q. 
U 

(55 



CO 



C/3 



u 






u 






2 


1) 


g 


1 


(fl 


o 


X 


u 


•"4 


1« 




u 


1 


'a 


<ll 


u 


CO 


a 



00 
< 



u 



ca — 

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582 



TABLE 92 



»^fnilhS[ON ICH*"uf SUHOI 



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Takeya Y, Popper JS, et al: Epidemiologic Studies of Coronary 
Heart Disease and Stroke in Japanese Men Living in Japan, Hawaii 
and California: Incidence of Stroke in Japan and Hawaii. 
Stroke 1984;15:15-23. 



583 



TABLE 93 



I 



Risk factor influence on distribution of stroke and coronary heart disease between geographic 
areas and tthnic groups with associated topography of vascular involvement and 

proposed model populations 





Risk factor 


Disease 




Class 


Blood 
lipid 
levels 


Blood 
pressure 


StTOlLC 


Coronary 
heart 
disease 


Model 
population 




Incideace 


Site of vascular lesion 


Incidence 




1 

2 
3 
4 


High 
High 
Low 
Low 


High 
Low 
High 
Low 


High 

Intermediate 
High 
Low 


Both intracranial and extracranial 
Mainly extracranial 
Mainly intracranial and intracerebral 
Few or none 


High 
High 
Low 
Low 


USA black 
USA white 
Japan 
Guatemala 



I 



Kuller L, Reisler DM: An explanation for variations in 
distribution of stroke and arteriosclerotic heart disease 
among populations and racial groups.' Am J Epidemiol 
1971;93:1-9. 



584 



"V.S. GOVERNMENT PRINTING OFFICE: 1986-620-638:'t07l6